Chloro(7,12-diethenyl-3,8,13,17-tetramethyl-21H,23H-porphine-2,18-dipropanoato(4-)-N(21),N(22),N(23),N(24)) ferrate(2-) dihydrogen.
The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins.
Porphyrins with four methyl, two vinyl, and two propionic acid side chains attached to the pyrrole rings. Protoporphyrin IX occurs in hemoglobin, myoglobin, and most of the cytochromes.
A mixed function oxidase enzyme which during hemoglobin catabolism catalyzes the degradation of heme to ferrous iron, carbon monoxide and biliverdin in the presence of molecular oxygen and reduced NADPH. The enzyme is induced by metals, particularly cobalt. EC
A ubiquitous stress-responsive enzyme that catalyzes the oxidative cleavage of HEME to yield IRON; CARBON MONOXIDE; and BILIVERDIN.
Proteins that contain an iron-porphyrin, or heme, prosthetic group resembling that of hemoglobin. (From Lehninger, Principles of Biochemistry, 1982, p480)
Salts and esters of the 7-carbon saturated monocarboxylic acid heptanoic acid.
A metallic element with atomic symbol Fe, atomic number 26, and atomic weight 55.85. It is an essential constituent of HEMOGLOBINS; CYTOCHROMES; and IRON-BINDING PROTEINS. It plays a role in cellular redox reactions and in the transport of OXYGEN.
The oxygen-carrying proteins of ERYTHROCYTES. They are found in all vertebrates and some invertebrates. The number of globin subunits in the hemoglobin quaternary structure differs between species. Structures range from monomeric to a variety of multimeric arrangements.
A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.
An acid dye used in testing for hydrochloric acid in gastric contents. It is also used histologically to test for AMYLOIDOSIS.
A species of gram-positive, asporogenous bacteria in which three cultural types are recognized. These types (gravis, intermedius, and mitis) were originally given in accordance with the clinical severity of the cases from which the different strains were most frequently isolated. This species is the causative agent of DIPHTHERIA.
Immature ERYTHROCYTES. In humans, these are ERYTHROID CELLS that have just undergone extrusion of their CELL NUCLEUS. They still contain some organelles that gradually decrease in number as the cells mature. RIBOSOMES are last to disappear. Certain staining techniques cause components of the ribosomes to precipitate into characteristic "reticulum" (not the same as the ENDOPLASMIC RETICULUM), hence the name reticulocytes.
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.
A species of gram-negative, anaerobic, rod-shaped bacteria originally classified within the BACTEROIDES genus. This bacterium produces a cell-bound, oxygen-sensitive collagenase and is isolated from the human mouth.
An enzyme of the transferase class that catalyzes condensation of the succinyl group from succinyl coenzyme A with glycine to form delta-aminolevulinate. It is a pyridoxyal phosphate protein and the reaction occurs in mitochondria as the first step of the heme biosynthetic pathway. The enzyme is a key regulatory enzyme in heme biosynthesis. In liver feedback is inhibited by heme. EC
Porphyrins which are combined with a metal ion. The metal is bound equally to all four nitrogen atoms of the pyrrole rings. They possess characteristic absorption spectra which can be utilized for identification or quantitative estimation of porphyrins and porphyrin-bound compounds.
A superfamily of proteins containing the globin fold which is composed of 6-8 alpha helices arranged in a characterstic HEME enclosing structure.
A diverse group of metabolic diseases characterized by errors in the biosynthetic pathway of HEME in the LIVER, the BONE MARROW, or both. They are classified by the deficiency of specific enzymes, the tissue site of enzyme defect, or the clinical features that include neurological (acute) or cutaneous (skin lesions). Porphyrias can be hereditary or acquired as a result of toxicity to the hepatic or erythropoietic marrow tissues.
The period from onset of one menstrual bleeding (MENSTRUATION) to the next in an ovulating woman or female primate. The menstrual cycle is regulated by endocrine interactions of the HYPOTHALAMUS; the PITUITARY GLAND; the ovaries; and the genital tract. The menstrual cycle is divided by OVULATION into two phases. Based on the endocrine status of the OVARY, there is a FOLLICULAR PHASE and a LUTEAL PHASE. Based on the response in the ENDOMETRIUM, the menstrual cycle is divided into a proliferative and a secretory phase.
An autosomal dominant porphyria that is due to a deficiency of HYDROXYMETHYLBILANE SYNTHASE in the LIVER, the third enzyme in the 8-enzyme biosynthetic pathway of HEME. Clinical features are recurrent and life-threatening neurologic disturbances, ABDOMINAL PAIN, and elevated level of AMINOLEVULINIC ACID and PORPHOBILINOGEN in the urine.
A group of metabolic diseases due to deficiency of one of a number of LIVER enzymes in the biosynthetic pathway of HEME. They are characterized by the accumulation and increased excretion of PORPHYRINS or its precursors. Clinical features include neurological symptoms (PORPHYRIA, ACUTE INTERMITTENT), cutaneous lesions due to photosensitivity (PORPHYRIA CUTANEA TARDA), or both (HEREDITARY COPROPORPHYRIA). Hepatic porphyrias can be hereditary or acquired as a result of toxicity to the hepatic tissues.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
One of the enzymes active in the gamma-glutamyl cycle. It catalyzes the synthesis of gamma-glutamylcysteine from glutamate and cysteine in the presence of ATP with the formation of ADP and orthophosphate. EC
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
Infections with bacteria of the family BACTEROIDACEAE.
A publication issued at stated, more or less regular, intervals.
A species of gram-negative bacteria in which man is the primary host and the human body louse, Pediculus humanus, the principal vector. It is the etiological agent of TRENCH FEVER.
Chronic delayed gastric emptying. Gastroparesis may be caused by motor dysfunction or paralysis of STOMACH muscles or may be associated with other systemic diseases such as DIABETES MELLITUS.
The evacuation of food from the stomach into the duodenum.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
c-Kit positive cells related to SMOOTH MUSCLE CELLS that are intercalated between the autonomic nerves and the effector smooth muscle cells of the GASTROINTESTINAL TRACT. Different phenotypic classes play roles as pacemakers, mediators of neural inputs, and mechanosensors.
Inorganic compounds that contain tin as an integral part of the molecule.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
A trace element that is required in bone formation. It has the atomic symbol Sn, atomic number 50, and atomic weight 118.71.
A strain of non-obese diabetic mice developed in Japan that has been widely studied as a model for T-cell-dependent autoimmune insulin-dependent diabetes mellitus in which insulitis is a major histopathologic feature, and in which genetic susceptibility is strongly MHC-linked.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
A yellow-orange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes.
A plant genus of the family ZINGIBERACEAE that contains CURCUMIN and curcuminoids.
A synthetic amino acid that depletes glutathione by irreversibly inhibiting gamma-glutamylcysteine synthetase. Inhibition of this enzyme is a critical step in glutathione biosynthesis. It has been shown to inhibit the proliferative response in human T-lymphocytes and inhibit macrophage activation. (J Biol Chem 1995;270(33):1945-7)
A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.
Techniques used for determining the values of photometric parameters of light resulting from LUMINESCENCE.
Antibodies that are chemically bound to a substrate material which renders their location fixed.
Nanometer-scale wires made of materials that conduct electricity. They can be coated with molecules such as antibodies that will bind to proteins and other substances.
5-Amino-2,3-dihydro-1,4-phthalazinedione. Substance that emits light on oxidation. It is used in chemical determinations.
The study of chemical changes resulting from electrical action and electrical activity resulting from chemical changes.
Emission of LIGHT when ELECTRONS return to the electronic ground state from an excited state and lose the energy as PHOTONS. It is sometimes called cool light in contrast to INCANDESCENCE. LUMINESCENT MEASUREMENTS take advantage of this type of light emitted from LUMINESCENT AGENTS.
An allotropic form of carbon that is used in pencils, as a lubricant, and in matches and explosives. It is obtained by mining and its dust can cause lung irritation.

delta-Aminolevulinate synthetases in the liver cytosol fraction and mitochondria of mice treated with allylisopropylacetamide and 3,5-dicarbethoxyl-1,4-dihydrocollidine. (1/964)

Hepatic delta-aminolevulinate (ALA) synthetase was induced in mice by the administration of allylisopropylacetamide (AIA) and 3,5-dicarbethoxy-1,4-dihydrocollidine (DDC). In both cases, a significant amount of ALA synthetase accumulated in the liver cytosol fraction as well as in the mitochondria. The apparent molecular weight of the cytosol ALA synthetase was estimated to be 320,000 by gel filtration, but when the cytosol ALA synthetase was subjected to sucrose density gradient centrifugation, it showed a molecular weight of 110,000. In the mitochondria, there were two different sizes of ALA synthetase with molecular weights of 150,000 and 110,000, respectively; the larger enzyme was predominant in DDC-treated mice, whereas in AIA-treated mice and normal mice the enzyme existed mostly in the smaller form. When hemin was injected into mice pretreated with DDC, the molecular size of the mitochondrial ALA synthetase changed from 150,000 to 110,000. The half-life of ALA synthetase in the liver cytosol fraction was about 30 min in both the AIA-treated and DDC-treated mice. The half-life of the mitochondrial ALA synthetase in AIA-treated mice and normal mice was about 60 min, but in DDC-treated mice the half-life was as long as 150 min. The data suggest that the cytosol ALA synthetase of mouse liver is a protein complex with properties very similar to those of the cytosol ALA synthetase of rat liver, which has been shown to be composed of the enzyme active protein and two catalytically inactive binding proteins, and that ALA synthetase may be transferred from the liver cytosol fraction to the mitochondria with a size of about 150,000 daltons, followed by its conversion to enzyme with a molecular weight of 110,000 within the mitochondria. The process of intramitochondrial enzyme degradation seems to be affected in DDC-treated animals.  (+info)

8-Aminoquinolines active against blood stage Plasmodium falciparum in vitro inhibit hematin polymerization. (2/964)

From the Walter Reed Army Institute of Research (WRAIR) inventory, thirteen 8-aminoquinoline analogs of primaquine were selected for screening against a panel of seven Plasmodium falciparum clones and isolates. Six of the 13 8-aminoquinolines had average 50% inhibitory concentrations between 50 and 100 nM against these P. falciparum clones and were thus an order of magnitude more potent than primaquine. However, excluding chloroquine-resistant clones and isolates, these 8-aminoquinolines were all an order of magnitude less potent than chloroquine. None of the 8-aminoquinolines was cross resistant with either chloroquine or mefloquine. In contrast to the inactive primaquine prototype, 8 of the 13 8-aminoquinolines inhibited hematin polymerization more efficiently than did chloroquine. Although alkoxy or aryloxy substituents at position 5 uniquely endowed these 13 8-aminoquinolines with impressive schizontocidal activity, the structural specificity of inhibition of both parasite growth and hematin polymerization was low.  (+info)

Identification of quinone-binding and heme-ligating residues of the smallest membrane-anchoring subunit (QPs3) of bovine heart mitochondrial succinate:ubiquinone reductase. (3/964)

The smallest membrane-anchoring subunit (QPs3) of bovine heart succinate:ubiquinone reductase was overexpressed in Escherichia coli JM109 as a glutathione S-transferase fusion protein using the expression vector pGEX2T/QPs3. The yield of soluble active recombinant glutathione S-transferase-QPs3 fusion protein was isopropyl-1-thio-beta-D-galactopyranoside concentration-, induction growth time-, temperature-, and medium-dependent. Maximum yield of soluble recombinant fusion protein was obtained from cells harvested 3.5 h post-isopropyl-1-thio-beta-D-galactopyranoside (0.4 mM)-induction growth at 25 degrees C in 2.0% tryptone, 0.5% yeast extract, 10 mM NaCl, 2.5 mM KCl, 10 mM MgCl2, 20 mM glucose (SOC medium) containing 440 mM sorbitol and 2.5 mM betaine. QPs3 was released from the fusion protein by proteolytic cleavage with thrombin. Isolated recombinant QPs3 shows one protein band in sodium dodecyl sulfate-polyacrylamide gel electrophoresis that corresponds to subunit V of mitochondrial succinate:ubiquinone reductase. Although purified recombinant QPs3 is dispersed in 0.01% dodecylmaltoside, it is in a highly aggregated form, with an apparent molecular mass of more than 1 million. The recombinant QPs3 binds ubiquinone, causing a spectral blue shift. Upon titration of the recombinant protein with ubiquinone, a saturation behavior is observed, suggesting that the binding is specific and that recombinant QPs3 may be in the functionally active state. Two amino acid residues, serine 33 and tyrosine 37, in the putative ubiquinone binding domain of QPs3 are involved in ubiquinone binding because the S33A- or Y37A-substituted recombinant QPs3s do not cause the spectral blue shift of ubiquinone. Although recombinant QPs3 contains little cytochrome b560 heme, the spectral characteristics of cytochrome b560 are reconstituted upon addition of hemin chloride. Reconstituted cytochrome b560 in recombinant QPs3 shows a EPR signal at g = 2.92. Histidine residues at positions 46 and 60 are responsible for heme ligation because the H46N- or H60N-substituted QPs3 fail to restore cytochrome b560 upon addition of hemin chloride.  (+info)

Urate synthesis in the blood-sucking insect rhodnius prolixus. Stimulation by hemin is mediated by protein kinase C. (4/964)

Hemin is a catalyst of the formation of reactive oxygen species. We proposed that hematophagous insects are exposed to intense oxidative stress because of hemoglobin hydrolysis in their midgut (Petretsky, M. D., Ribeiro, J. M. C., Atella, G. C., Masuda, H., and Oliveira, P. L. (1995) J. Biol. Chem. 270, 10893-10896). We have shown that hemin stimulates urate synthesis in the blood-sucking insect Rhodnius prolixus (Graca-Souza, A. V., Petretsky, J. H., Demasi, M., Bechara, E. J. H., and Oliveira, P. L. (1997) Free Radical Biol. Med. 22, 209-214). Once released by fat body cells, urate accumulates in the hemolymph, where this radical scavenger constitutes an important defense against blood-feeding derived oxidative stress. Incubation of Rhodnius fat bodies with okadaic acid raises the level of urate synthesis, suggesting that urate production can be controlled by protein phosphorylation/dephosphorylation. Urate synthesis is stimulated by dibutyryl cAMP and inhibited by N(2((p-bromocinnamil)amino)ethyl)-5-isoquinolinesulfonamide (H-89), an inhibitor of protein kinase A, as well as activated by the protein kinase C activator phorbol 12-myristate 13-acetate. In the presence of hemin, however, inhibition of urate synthesis by H-89 does not occur, suggesting that the hemin stimulatory effect is not mediated by protein kinase A. Calphostin C completely inhibits the hemin-induced urate production, suggesting that the triggering of urate antioxidant response depends on protein kinase C activation. This conclusion is reinforced by the observation that in fat bodies exposed to hemin, both protein kinase C activity and phosphorylation of specific endogenous polypeptides are significantly increased.  (+info)

Phosphatidylserine externalization during differentiation-triggered apoptosis of erythroleukemic cells. (5/964)

K562 erythroleukemia cells undergo apoptosis when induced to differentiate along the erythroid lineage with hemin. This event, characterized by DNA fragmentation, correlated with downregulation of the survival protein, BCL-xL, and decrease in mitochondrial transmembrane potential (deltapsi[m]) that ultimately resulted in cell death. Reorientation of phosphatidylserine (PS) from the cells inner-to-outer plasma membrane leaflet and inhibition of the aminophospholipid translocase was observed upon hemin-treatment. Constitutive expression of BCL-2 did not inhibit hemin-induced alterations in lipid asymmetry or decrease in deltapsi[m], and only moderately prevented DNA fragmentation. BCL-2, on the other hand, effectively inhibited actinomycin D-induced DNA fragmentation, the appearance of PS at the cells outer leaflet and the decrease in deltapsi[m]. The caspase inhibitor, z.VAD.fmk, blocked DNA fragmentation by both hemin and actinomycin D, but inhibited PS externalization only in the actinomycin D-treated cells. These results suggest that, unlike pharmacologically-induced apoptosis, PS externalization triggered by differentiation-induced apoptosis occurs by a mechanism that is associated with a decrease in deltapsi[m], but independent of BCL-2 and caspases.  (+info)

The haemin storage (Hms+) phenotype of Yersinia pestis is not essential for the pathogenesis of bubonic plague in mammals. (6/964)

The haemin storage (Hms+) phenotype of Yersinia pestis enables this bacillus to form greenish/brown or red colonies on haemin or Congo Red agar plates, respectively, at 26 but not 37 degrees C. Escherichia coli strains that contain mutations in genes essential for siderophore biosynthesis, porphyrin generation and/or haemin transport remain unable to utilize exogenous haemin as a nutritional iron or porphyrin source when transformed with the cloned Y. pestis hmsHFRS locus. Further physiological analysis of the Hms+ phenotype of Y. pestis strain KIM6+ suggests that the haemin and inorganic iron stored by the Hms system was not used nutritionally under subsequent iron-deficient conditions. In vitro analysis of the bactericidal effects of hydrogen peroxide, superoxide and nitric oxide showed that Hms- Y. pestis cells, in certain cases, were more susceptible than the Hms+ parent cells to these reactive oxygen species at 26 and/or 37 degrees C. In adherence assays, a higher percentage of Hms+ cells were associated with HeLa cells and normal human neutrophils, compared to Hms- cells. However, the Hms+ phenotype did not provide any additional protection against the killing effects of neutrophils. Finally, LD50 analysis in subcutaneously infected mice showed that an Hms- strain was slightly more virulent than Hms+, indicating that the Hms phenotype is not essential for the pathogenesis of bubonic plague in mammals.  (+info)

Cellular uptake of chloroquine is dependent on binding to ferriprotoporphyrin IX and is independent of NHE activity in Plasmodium falciparum. (7/964)

Here we provide definitive evidence that chloroquine (CQ) uptake in Plasmodium falciparum is determined by binding to ferriprotoporphyrin IX (FPIX). Specific proteinase inhibitors that block the degradation of hemoglobin and stop the generation of FPIX also inhibit CQ uptake. Food vacuole enzymes can generate cell-free binding, using human hemoglobin as a substrate. This binding accounts for CQ uptake into intact cells and is subject to identical inhibitor specificity. Inhibition of CQ uptake by amiloride derivatives occurs because of inhibition of CQ-FPIX binding rather than inhibition of the Na+/H+ exchanger (NHE). Inhibition of parasite NHE using a sodium-free medium does not inhibit CQ uptake nor does it alter the ability of amilorides to inhibit uptake. CQ resistance is characterized by a reduced affinity of CQ-FPIX binding that is reversible by verapamil. Diverse compounds that are known to disrupt lysosomal pH can mimic the verapamil effect. These effects are seen in sodium-free medium and are not due to stimulation of the NHE. We propose that these compounds increase CQ accumulation and overcome CQ resistance by increasing the pH of lysosomes and endosomes, thereby causing an increased affinity of binding of CQ to FPIX.  (+info)

Peroxynitrite induces haem oxygenase-1 in vascular endothelial cells: a link to apoptosis. (8/964)

Peroxynitrite (ONOO-) is a potent oxidizing agent generated by the interaction of nitric oxide (NO) and the superoxide anion. In physiological solution, ONOO- rapidly decomposes to a hydroxyl radical, one of the most reactive free radicals, and nitrogen dioxide, another species able to cause oxidative damage. In the present study we investigated the effect of ONOO- on the expression of haem oxygenase-1 (HO-1), an inducible protein that is highly up-regulated by oxidative stress. Exposure of bovine aortic endothelial cells to ONOO- (250-1000 microM) produced a concentration-dependent increase in haem oxygenase activity and HO-1 protein expression. This effect was completely abolished by the ONOO- scavengers uric acid and N-acetylcysteine, and partly attenuated by 1,3-dimethyl-2-thiourea, a scavenger of hydroxyl radicals. ONOO- also produced a concentration-dependent increase in apoptosis and cytotoxicity, which were considerably decreased by uric acid and N-acetylcysteine. A 70% decrease in apoptosis was observed when cells were exposed to ONOO- in the presence of 10 microM tin protoporphyrin IX (SnPPIX), an inhibitor of haem oxygenase activity. When SnPPIX was added 5 min after ONOO-, apoptosis decreased by only 40%, which suggests that an interaction between ONOO- and the protoporphyrin occurs in our system. Increased haem oxygenase activity by pretreatment of cells with haemin resulted in elevated bilirubin production and was associated with a substantial decrease (35%) in ONOO--mediated apoptosis. These results indicate the ability of ONOO- to modulate the expression of the stress protein HO-1 and suggest that the haem oxygenase pathway contributes to protection against the cytotoxic action of ONOO-.  (+info)

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Curcumin is a bifunctional antioxidant derived from |i|Curcuma longa|/i|. This study identifies curcumin as a neuroprotectant against hemin-induced damage in primary cultures of cerebellar granule neurons (CGNs) of rats. Hemin, the oxidized form of heme, is a highly reactive compound that induces cellular injury. Pretreatment of CGNs with 5–30 |i|μ|/i|M curcumin effectively increased by 2.3–4.9 fold heme oxygenase-1 (HO-1) expression and by 5.6–14.3-fold glutathione (GSH) levels. Moreover, 15 |i|μ|/i|M curcumin attenuated by 55% the increase in reactive oxygen species (ROS) production, by 94% the reduction of GSH/glutathione disulfide (GSSG) ratio, and by 49% the cell death induced by hemin. The inhibition of heme oxygenase system or GSH synthesis with tin mesoporphyrin and buthionine sulfoximine, respectively, suppressed the protective effect of curcumin against hemin-induced toxicity. These data strongly suggest that HO-1 and GSH play a
The present study demonstrates a function of HO-1 activity as a potent host defense factor for HIV-1 infection. Our results clearly show that activation of HO-1 by its substrate hemin protected them against HIV infection with various clinical HIV isolates, including some of those that developed resistance to conventional antiretroviral drugs. In vivo, hemin administration in humanized NOD-SCID mice substantially suppressed HIV replication. These findings suggest that the HO-1 inducer, hemin, is a potentially effective endogenous biologic in inducing a host defense response against HIV infection. A critical component of a variety of proteins, including hemoglobin, hemin has been shown to exert numerous beneficial physiological functions (25). After being approved by the Food and Drug Administration, several formulations of hemin have been used since the 1970s to successfully treat acute porphyries, to control liver allograft failure due to recurrence of erythopoietic protophoria, and in patients ...
TY - JOUR. T1 - Hemin induces neuroglobin expression in neural cells. AU - Zhu, Yonghua. AU - Sun, Yunjuan. AU - Jin, Kunlin. AU - Greenberg, David A.. PY - 2002/10/1. Y1 - 2002/10/1. N2 - Neuroglobin is a newly identified vertebrate globin that binds O2 and is expressed in cerebral neurons. We found recently that neuronal expression of neuroglobin is stimulated by hypoxia and ischemia and protects neurons from hypoxic injury. Here we report that, like hemoglobin and myoglobin, neuroglobin expression can also be induced by hemin. Induction was concentration dependent and time dependent, with maximal (about 4-fold) increases in neuroglobin mRNA and protein levels occurring with 50 μM hemin and at 8 to 24 hours. The inductive effect of hemin was attenuated by the protein kinase G inhibitor KT5823 and the soluble guanylate cyclase inhibitor LY83583, was mimicked by treatment with 8-bromo-cyclic guanosine 3′,5′-monophosphate, and was accompanied by a greater than 10-fold increase in cGMP ...
Hemin is made of red blood cells processed from human blood. Hemin works by lowering the production of a certain enzyme in the body. Hemin is used to treat the symptoms of occasional attacks of porphyria related to the menstrual cycle in women. Hemin helps control symptoms such as pain, increased heart rate or blood...
Different pharmacological and genetic approaches have been used to upregulate HO-1 with the ultimate goal of normalization of BP in SHRs.5,7 The usage of stannous chloride for 4 days (IP), a well-known HO inducer, significantly lowered BP of 7-week-old SHRs but not that of 20-week-old SHRs.6 Treatment with hemin and hemin arginate of 7-week-old SHRs for 4 days (IP) normalized high systolic BP to 130±5 mm Hg.11 Systolic BP of these rats reached 140 mm Hg 1 week later and gradually increased to the levels of untreated SHRs 1 month later.11 All of these previous attempts to combat hypertension by upregulating HO only modestly lowered high BP in young SHRs (5 to 8 weeks old) for an apparently short period of time (3 to 4 weeks).12 Once hypertension is fully established in SHRs (such as in 20-week-old SHRs), upregulating HO expression using a 4-day IP hemin injection failed to lower BP.5,13,14 More importantly, a long-lasting normalization of BP in the absence of antihypertensive interventions has ...
In this study we report the activation of c-Jun N-terminal kinase (JNK) in human K562 erythroleukemia cells undergoing hemin-mediated erythroid differentiation, which occurs concomitantly with activation of heat shock factor 2 (HSF2) and leads to a simultaneous in vivo phosphorylation of c-Jun. The activation of JNK occurs through activation of mitogen-activated protein kinase kinase (MKK) 4 and not by activation of MKK7 or inhibition of JNK-directed phosphatases. We have previously shown that overexpression of the HSF2-beta isoform inhibits the activation of HSF2 upon hemin-induced erythroid differentiation. Here we demonstrate that HSF2-beta overexpression blocks the hemin-induced activation of the MKK4-JNK pathway, suggesting an erythroid lineage-specific JNK activation likely to be regulated by HSF2. ...
Hasan and Schafer demonstrate that hemin-induced Egr-1 expression is derived solely from its ability to induce ROS. Using a panel of ROS scavengers and inhibitors, the authors show that superoxide is necessary for Egr-1 induction because the superoxide scavenger, tiron, completely inhibits hemin-induced ROS. Inhibition of NADPH oxidase activity with apocynin also completely abolishes hemin-induced ROS. Confirmation of these results using alternate approaches such as genetically targeted models or small interfering RNA knockdown will further strengthen the role of NADPH oxidase. These results are significant because they demonstrate that increased ROS levels may be a consequence of the activation of NADPH oxidase by heme and not the result of Fe2+ toxicity. This suggests that heme remains intact in VSM under experimental conditions, eliminating a role for HO-1 and other degradation products, CO and biliverdin/bilirubin, and also excludes the nonenzymatic oxidative degradation of heme and the ...
This paper reviews the evidence that protein synthesis in rabbit reticulocytes is regulated by the reversible phosphorylation of the initiation factor eIF-2 by protein kinases under the control of the cytoplasmic haemin concentration on the one hand, and double-stranded RNA on the other. A molecular mechanism is proposed to account for the observation that inhibition of protein synthesis occurs when considerably less than half the eIF-2 present has been phosphorylated. The question of whether phosphorylation regulates protein synthesis in other types of cell is discussed. ...
Аннотация доклада: Efforts to replace native peroxidase with its low molecular weight alternatives have stimulated a search for peroxidase mimetics. Herein we describe the oxidation of luminol with hydrogen peroxide catalyzed by commercial available FeIII-TAML activator 1a, which was showed to be more active catalyst than hemin. At FeIII-TAML activator 1a use in chemiluminescent assay for H2O2 determination the limit value (3σ) was 5 x 10-8 M, whereas in the presence of hemin the detection limit was significantly higher and equal to 6 x 10-7 M. The linear ranges (R2 = 0.98) of the assay were 6 x 10-8 - 1 x 10-6 M and 6 x 10-7 - 1 x 10-6 M H2O2 for FeIII-TAML 1a and hemin, respectively. The CV values for FeIII-TAML 1a-based assay measured within the working range varied from 1.0 to 3.7 % (n=4), whereas in the case of hemin - 5.0 to 9.7 % (n=4). Moreover, the sensitivity of FeIII-TAML 1a-based method was 56 times higher than that of hemin-based method. The obtained results open ...
BOMBICINI, R L; SCHMITT, T H; FREZZATI JUNIOR, W A; SCHREIER, Shirley. Effect of hemin upon structure, permeability and peroxidation of membranes. Arquivos de Biologia e Tecnologia[S.l: s.n.], 1986 ...
s including MARHS4, MARHS2 and MARe in uninduced K562 cells. Hemin induction of the K562 cells obviously increased the binding of SATB1 to MARHS4, MARHS2 and
Abstract: The DNA oligonucleotide PS2.M has been previously reported to have nanomolar affinity for hemin. The PS2.M-hemin complex then exhibits peroxidase activity. It was predicted that this sequence could be used in a catalytic beacon to facilitate the development of a laboratory tool that would be effective at determining potential siRNA target sites. The PS2.M-based beacon used for this study forms a stem-loop structure that opens upon hybridization with a single-stranded target sequence. Once open, the PS2.M part of the beacon can fold, locking hemin within a three level planer arrangement. Once hemin is in place, the structure is catalytically active and can catalyze the oxidization of the chromogenic substrate 2,2,-azino-bis (3-ethylebenzthiazoline-6-sulphonic acid) (ABTS) in the presence of hydrogen peroxide. Thus, binding of the beacon can be monitored with absorbance readings at 414 nm. Although molecular beacons with a stem-loop structure could potentially be used for this type of ...
Iron acquisition and metabolismIron acquisition and metabolism - no subcategoryHeme, hemin uptake and utilization systems in GramPositives Uncharacterized siderophore biosynthesis protein near heme transporter HtsABC ...
Iron acquisition and metabolismIron acquisition and metabolism - no subcategoryHeme, hemin uptake and utilization systems in GramPositives Iron compound ABC uptake transporter permease protein ...
Although heme oxygenase-1 and glutathione play important roles in the antioxidant defense system, the sharing and/or cross-talking of the HO-1 and GSH system remain poorly understood. The object of this study is to determine whether the glutathione system is involved in the antioxidant function of hemin. Hydrogen peroxide decreased the viability of the human leukemic monocyte lymphoma cell line U937. When these cells were pretreated with hemin before the addition of hydrogen peroxide, cell death was prevented. An inhibitor of heme oxygenase-1 or glutathione biosynthesis significantly abolished this protective effect of hemin. These results suggest that both heme oxygenase-1 and glutathione are involved in the protective effects of hemin against U937 cell death, which was induced by hydrogen peroxide. Hemin induced an increase in glutathione levels following the upregulation of the gene expression and protein levels of glutamate-cysteine ligase catalytic subunit. The inhibitor of heme oxigenase-1
Therapeutic options for management of diabetic gastroparesis are limited. Failure to maintain upregulation of heme oxygenase 1 (HO1) leads to loss of interstitial cells of Cajal and delayed gastric emptying in diabetic non-obese diabetic mice.. HO1 is an enzyme which protects cells from physical, chemical, and biologic stress. In mice with diabetes and slow gastric emptying, hemin increases HO-1 activity and improves gastric emptying. Hemin is produced from red blood cells and is approved by the Food and Drug Administration for treating acute porphyria, which is an inherited condition caused by an enzyme deficiency. Hemin is not approved by the Food and Drug Administration for treating gastroparesis.. In this study subjects were randomized to intravenous hemin, prepared in albumin, or albumin alone. After infusions on days 1, 3, and 7, weekly infusions were administered for 7 weeks. Assessments included blood tests for HO1 protein and enzyme activity levels, gastric emptying with 13^C-spirulina ...
An acid-base interaction between hemin and PAMAM dendrimers affords supramolecular non-covalent peroxidase systems whose catalytic activity is enhanced after spontaneous electrostatic self-assembling onto a solid surface ...
Neisseria gonorrhoeae, the etiologic agent of gonorrhea, utilizes TonB-dependent transporters to import essential nutrients such as iron. Study of TonB-dependent transporters is extremely important due to the fact that they make excellent vaccine targets. In order to learn more about the structure, function, expression, and regulation of selected TonB-dependent transporters, three goals were established for this study. The first goal was to examine the role of two highly conserved regions of TbpB in lipidation. One of the conserved regions of TbpB, the LSAC motif, was shown to be critical for lipidation. The second goal was to determine whether MisR/MisS regulates expression of TbpA and TbpB. MisR/MisS was shown to regulate the expression of TbpA and TbpB. The third goal was to assess the ability of recombinant TdfJ to bind hemin when expressed in E. coli. Recombinant TdfJ was shown to specifically bind hemin when expressed in E. coli.
Figure 2. Dependency of hemin catabolism on riboflavin bioavailability. The elimination of hemin requires cyclic reduction of heme oxygenase by flavoprotein cytochrome P450 reductase that, in turn, utilizes both flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD) as prosthetic groups. Average or increased red meat consumption may overload the capacity of this chain of reactions already compromised by impaired intestinal absorption of riboflavin (with decreased FMN and FAD synthesis), leading to increased hemin (iron) delivery to the CNS and increased utilization of riboflavin for hemin inactivation. Modified from Figure 1, box 21-1, page 783 of Ref. 2 ...
The implications of this research, identify hemin as a potential therapeutic target for sporadic Creutzfeldt-Jakob disease (CJD) and cerebral hemorrhage.
1. Pyridine reacts with alkaline haematin to form a dipyridine dihydroxy dimeric haematin in which there is no competition between pyridine and OH− for coordination positions on the iron of haematin. 2. Imidazole competes directly with OH− to form the monomeric imidazole parahaematin in alkaline media. 3. The monomeric imidazole parahaematin aggregates readily to form a species that is precipitated on standing. 4. A structure is proposed for the haematin-pyridine compound in alkaline media.. ...
In the course of a general study of the structure of hemoglobin and its derivatives we have investigated the magnetic properties of ferriheme, ferroheme, several hemochromogens and nickel protoporphyrin. The results of this investigation and their structural interpretation are discussed in the following paragraphs.. The prosthetic group of hemoglobin, ferrous protoporphyrin, we call ferroheme, ferriheme being ferric protoporphyrin combined with a negative ion (chloride in hemin, hydroxide in hematin). On denaturation hemoglobin forms a deep red substance called hemochromogen.1 It was shown by Anson and Mirsky2 in 1925 that hemochromogen is not ferroheme itself, as had been thought before, but a compound of ferroheme and denatured globin, and that hemochromogens in general are compounds of ferroheme and other substances, usually containing nitrogen. The characteristic property of the hemochromogens is their strong absorption spectrum of two sharp bands, α at about 5600 Å and β at about 5200 ...
Comments to the paper Observations on the Alkaline Haematin/Detergent Complex for Measuring Haemoglobin Concentration by O. W. van Assendelft and W. G. Zijlstra (1 ...
Lee, Heung-Man; Park, Il-Ho; Shin, Jae-Min; Yoon, Hyun-Sun; Park, Gyeong Yul; Zeher, Margit; Matsui, Katsuhiko; Tamai, Saki; Ikeda, Reiko; Suri, Drsushil; Suri, Dranu; Arani, Marzieh Heidarzadeh; Lubis, Azwin; Endaryanto, Anang; Koga, Shinichiro; Suk, Lee Ju; Tsuzuki, Yasunobu; Kim, Seo Hyeong; Shin, Jung U.; Noh, Ji Yeon; Jin, Shan; Jin, Shan; Lee, Hemin; Lee, Jungsoo; Park, Chang Ook; Lee, Kwang Hoon; Lee, Kwang Hoon; Tepetam, Fatma Merve; Park, Chun Wook; Son, Jee Hee; Cho, Soo Ick; Cho, Yong Se; Byun, Yun Sun; Yang, Yoon Seok; Chung, Bo Young; Kim, Hye One; Cho, Hee Jin; Katada, Yoshinori; Tanaka, Toshio; Nakabayashi, Akihiko; Nishida, Koji; Aoyagi, Kenichi; Tsukamoto, Yuki; Konma, Kazushi; Matsuura, Motoo; Park, Jung-Won; Harada, Yoshinori; Jeong, Kyoung Yong; Yura, Akiko; Yoshimura, Maiko; Kyung, Tae-Suk; Kim, Young Hyo; Park, Chang-Shin; Jang, Tae Young; Heo, Min-Jeong; Jung, Ah-Yeoun; Yang, Seung-Chan; Kim, Hye One; Cho, Yong Se; Byun, Yun Sun; Yang, Yoon Seok; Chung, Bo Young; Son, Jee ...
Purpose: Diabetic retinopathy (DR) is a progressive neurodegenerative disease and a leading cause of blindness. Overexpression of Heme Oxygenase-1(HO-1) by hemin induction protected retinal ganglion cells in diabetic retinopathy through anti-inflammatory, anti-apoptotic, and anti-proliferative effects. We investigated microRNA (miRNA) alterations in DR after hemin treatment with specific focus on miR-126, and its downstream target, HO-1.. Methods: miRNA expression profiling microarray (Affymetrix MicroRNA 2.0 Array) was used to examine the retinas of treated and non-treated streptozotocin- induced diabetic rats. Expressions of specific miRNAs were verified with PCR in the rat retina and in glucose-exposed endothelial cells. A target search, based on sequence complementarities, identified specific targets. We analyzed mRNA levels and protein expression in endothelial cells from large vessels and retinal capillaries and in the rat retina, with or without injection of miR-126 mimic or antagomir. ...
Post-liver transplantation acute lung injury (ALI) severely affects patients survival, whereas the mechanism is unclear and effective therapy is lacking. The authors postulated that reperfusion-induced increased oxidative stress plays a critical role in mediating post-liver transplantation ALI and that induction of heme oxgenase-1 (HO-1), an enzyme with anti-oxidative stress properties, can confer effective protection of lung against ALI. Male Sprague-Dawley rats underwent autologous orthotopic liver transplantation (OALT) in the absence or presence of treatments with the selective HO-1 inducer (Hemin) or HO-1 inhibitor (ZnPP). Lung tissues were collected at 8 h after OALT, pathological scores and lung water content were evaluated; survival rate of rats was analyzed; protein expression of HO-1 was determined by western blotting, and nuclear translocation of Nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor(NF)-κB p65 were detected by Immunofluorescence staining. The inflammatory
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Objective(s):Fuzheng Huayu recipe (FZHY) exerts significant protective effects against liver fibrosis by strengthening the bodys resistance and removing blood stasis. However, the molecular mechanisms through which FZHY affects liver fibrosis are still unclear. In this study, we examined the expression levels of factors involved in the inhibitor κB kinase-β (IKK-β)/nuclear factor-κB (NF-κB) and transforming growth factor beta 1 (TGF-β1)/Smad signaling pathways to elucidate whether FZHY could attenuate nutritional steatohepatitis and fibrosis in mice. Materials and Methods: C57BL/6J mice were fed with methionine-choline deficient (MCD) diet for 8 weeks to induce fibrotic steatohepatitis. FZHY and/or heme oxygenase-1 (HO-1) chemical inducer (hemin) were administered to mice. The effects of FZHY alone and in combination with hemin were assessed by comparing the severity of hepatic injury, activation of hepatic stellate cells (HSCs), and the expression of oxidative stress, inflammation and
Cairan empedu berasal dari penghancuran hemoglobin dari eritrosit yang telah tua. Hemoglobin ini akan di uraikan menjadi hemin, zat besi, dan globin. Zat besi dan globin akan di simpan di dalam hati kemudian di kirim ke sum-sum tulang merah. Zat-zat tersebut digunakan dalam pembentukan antibodi atau hemoglobin baru. Sementara itu, Hemin akan di rombak menjadi bilirubin dan biliverdin. Bilirubin dan biliverdin ini merupakan zat warna bagi empedu dan mengandung warna hijau-biru. Zat warna tersebut di dalam usus akan mengalami oksidasi menjadi urobilin. Urobilin kemudian di eksresikan dari dalam tubuh dan memberi warna kekuningan pada feses dan urine ...
4JES: The Hemophore HasA from Yersinia pestis (HasAyp) Coordinates Hemin with a Single Residue, Tyr75, and with Minimal Conformational Change.
Hemolytic anemia is one of the hallmarks of malaria and leads to an increase in oxidized heme (hemin) within the plasma of infected individuals. While scavenger proteins sequester much of the circulating heme, it has been hypothesized that extracellular heme may play a central role in malaria pathogenesis. W CSC100: Celebrating Canadian Chemistry
The preparation from ferriprotoporphyrin IX (FP) in aqueous acid medium of the related pigments beta- and B-hematin [see G. Blauer and M. Akkawi, Biochem. Mol. Biol. Int. 35, 231 (1995)] is presented under different conditions. Both pigments are characterized by infrared spectra which differ in the range of 1600-1700 cm-1 in their strong bands with absorption peaks measured at 1648 +/- 2 cm-1 for B-hematin and at 1663 +/- 1 cm-1 for beta-hematin. The pH dependence of B-hematin formation at 37 degrees C and at different concentrations of acetic acid and FP exhibits a maximum yield near pH 4. The formation of beta-hematin at 70 degrees C shows high yield in 6 M acetic acid or in the presence of 0.028 M trichloroacetate at pH 4.6. The dependence of the yield of the pigments on the time and temperature of incubation, concentration of FP, and the presence of different electrolytes was investigated. Both B- and beta-hematin are either insoluble or very slightly soluble in different solvents at room
1.3 mg/day. Therefore, if the PD patients had a normal absorptive capacity for vitamin B2, their large ingestion of red meat (up to 700 g/day), associated with milk, rice and beans, fruits and vegetables, should have provided a normal riboflavin status. In contrast, 31 consecutive PD patients had laboratory evidence for riboflavin deficiency (Table 2) suggesting that patients with sporadic PD belong to the subset of the general population (10-15%) (3) that may express a flavokinase with low affinity for vitamin B2, leading to a decreased absorption.. However, the digestion of red meat releases hemin, a highly diffusible toxin that, when not properly inactivated, increases intracellular iron concentrations and enhances hydroxyl radical production (Fenton reaction). Most of the absorbed hemin is destroyed by the enzyme heme oxygenase (HO) in the digestive tract and liver (26). Because HO is oxidized during the catabolization of hemin to biliverdin, the HO molecules must be reduced through the ...
The role of heme in the regulation of δ-aminolevulinic acid (ALA) synthetase was studied in fetal rat liver. The activity of ALA synthetase, the first and rate-limiting enzyme in the heme-biosynthetic pathway, is 10 times higher in fetal rat liver mitochondria than in adults. Hemin injection depresses mitochondrial ALA synthetase activity in the adult but not in the fetus. Cycloheximide, a selective inhibitor of protein synthesis in cytoplasmic ribosomes, but not in mitochondria, causes a rapid decrease in fetal mitochondrial ALA synthetase activity. When hemin is given prior to cycloheximide, a slower rate of turnover of mitochondrial ALA synthetase activity occurs than after cycloheximide alone. Treatment with 3-amino-1,2,4-triazole, an inhibitor of δ-aminolevulinic acid dehydratase, the second enzyme in heme biosynthesis, causes a decrease in fetal mitochondrial ALA synthetase activity but no decrease in the extramitochondrial enzyme levels. These studies indicate that heme may facilitate ...
1. Wheatgrass Juice is one of the best sources of living chlorophyll available today. However, to get the full benefit, the chlorophyll must come fresh from a living plant.. 2. Wheatgrass juice contains up to 70% chlorophyll, which is an important blood builder. The chlorophyll molecules closely resemble that of the hemin molecule, the pigment which combines with protein to form hemoglobin. The major difference is the chlorophyll molecule contains magnesium as its central atom, and the hemin molecule contains iron. The molecular structure of these two substances is almost identical in all other respects.. 3. Chlorophyll is the molecule that absorbs sunlight and uses its energy to synthesize carbohydrates from CO2 and water. This process is known as photosynthesis, a complex biochemical pathway in which solar energy is used to convert water and carbon dioxide to glucose and other carbohydrates, and is the basis for sustaining the life processes of all plants. Since animals and most humans obtain ...
If you have a question about this talk, please contact Frida Kaori Weierud.. Abstract not available. This talk is part of the Foster Talks series.. ...
may be the causative agent from the biphasic human being disease Oroya fever. Oxidative tension (1 mM H2O2) and hemin restriction got no significant influence SRSF2 on mRNA amounts. Dedication of proteins quantities using immunoblotting and SDS-PAGE showed the best levels of under acidic circumstances or in 20 °C. The least quantity of was synthesized […]. ...
Theresa2021-09-11T08:22:40-06:00September 10th, 2021,. MORE INCENTIVES FOR OWNERSHIP FOR THE 2022 SEASON! The HBPA of Albertas Directors are excited to announce the following program to our eligible participants starting in 2022. The HBPA may amend the program from time ...
Heme oxygenase-1 (HO-1), an antioxidant defense enzyme, has been shown to protect against oxidant-induced liver injury. However, its role on liver fibrosis remains unclear. This study aims to elucidate the effect and the mechanism of HO-1 in nutritional fibrosing steatohepatitis in mice. Male C57BL/6J mice were fed with a methionine-choline deficient (MCD) diet for eight weeks to induce hepatic fibrosis. HO-1 chemical inducer (hemin), HO-1 chemical inhibitor zinc protoporphyrin IX (ZnPP-IX) and/or adenovirus carrying HO-1 gene (Ad-HO-1) were administered to mice, respectively. Liver injury was assessed by serum ALT, AST levels and histological examination; hepatic lipid peroxides levels were determined; the expression levels of several fibrogenic related genes were assayed by real-time quantitative PCR and Western blot. MCD feeding mice showed progressive hepatic injury including hepatic steatosis, inflammatory infiltration and fibrosis. Induction of HO-1 by hemin or Ad-HO-1 significantly attenuated the
INTRODUCTION: Remifentanil preconditioning (RPC) can protect the heart from ischemia-reperfusion injury (IRI). Heme oxygenase-1 (HO-1) can also reduce the cardiac infarct size during ischemia reperfusion in vivo. Our aim was to investigate whether HO-1 expression participates in RPC cardio protection. METHODS: IRI was induced in male Sprague-Dawley rats (300g) by occluding the left coronary artery for 30 minutes followed by 2 hours of reperfusion. 6μg/kg/min remifentanil as administered in three infusion cycles of 5-min (RPC group). Hemin, an agonist of HO-1, 30mg/kg/d was given intraperitoneally for 2 days before RPC (RPC+hemin group). Tin Protoporphyrin IX (SnPP), which can inhibit HO-1 expression, was injected 0.7 mg/kg/day subcutaneously for 2 days before RPC (RPC+SnPP group). The non-operation group was marked as sham. In the control group, 0.9% saline replaced remifentanil. After the operation, the heart infarct size was determined by 2, 3, 5-triphenyltetrazolium staining. Expression of ...
target_id = 014432 $split = ___ $target = array( Target => array( id => 14861, target_id => 014432, local_target_id => 014432, locus_tag => RHE_CH03268, ncbi_gi => 86282969, ncbi_accession => ABC92032.1, ncbi_geneid => null, ncbi_taxon_id => 347834, gene_name => hmuS, common_name => hemin transport system, degrading protein [Rhizobium etli CFN 42], ncbi_coded_by_region => CP000133.1:3430983..3432032, ncbi_note => similar to HmuS [Rhizobium leguminosarum] and hmuS (SMc01513) [Sinorhizobium meliloti]; Similar to entrez-protein:CAC34392.1; Putative location:bacterial cytoplasm Psort-Score: 0.4277, tigr_main_role_id => null, tigr_sub_role_id => null, comment => null, justification => Symbiotic and global nitrogen fixation based on ortholog expansion from Sinorhizobium, sequence => ...
Dashper, S. G. et al Characterization of a Novel Outer Membrane Hemin-Binding Protein of Porphyromonas gingivalis . Journal of Bacteriology 182.22 (2000): 6456-6462. Web. 20 Nov. 2019. ...
There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining ...
Additional comment: After the equilibration, the IPG gel strips were cut to size. Six mm were removed from the anodic end and 14 mm from the cathodic end. The second dimension gels were overlayered with a solution containing agarose (0.5% w/v) and Tris-glycine-SDS (25 mM-198 mM-0.1% w/v) pH 8.3 heated at about 70o C and the IPG gel strips were immediately loaded through it ...
There are 11 seven-letter words containing A, H, M, N and T: ANTHEMS HEMATIN HETMANS ... PHANTOM THIAMIN XANTHAM. Every word on this site can be played in scrabble. Create other lists, that begin with or end with letters of your choice.
Talk Title: Pulse Azidohomoalanine (AHA) Labeling in Mammals (PALM) Analysis for Global Analysis of Newly-synthesized Proteins in Animal Models of Disease. VIEW MORE. ...
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Differentiation in murine erythroleukemic cells is arrested at the proerythroblast stage. A small fraction of the population, however, undergoes spontaneous differentiation. This spontaneous differentiation was examined at the individual cell level in relation to cell multiplication, commitment, and maturation. The results indicate that murine erythroleukemic cells destined to undergo spontaneous differentiation first undergo commitment, an irreversible process characterized by cells becoming (a) capable of producing hemoglobin coupled with (b) a loss of their ability to undergo more than six subsequent cell divisions. Commitment is followed by a maturation process which includes the accumulation of erythroid specific markers, e.g., hemoglobin. With respect to commitment, spontaneous differentiation resembles the differentiation produced by most inducers but differs from that evoked by hemin. Serum hemin may therefore be exempt from implication in the spontaneous process. ...
Our understanding of heme sensing and the regulation of heme-iron acquisition by fungal pathogens is incomplete. Heme contains ∼80% of the iron in vertebrate hosts, and we previously demonstrated that heme is an important iron source for C. neoformans (35, 74). In the present study, we constructed a strain encoding a cytosolic heme sensor to address our goals of (i) understanding heme-iron acquisition during fungal proliferation and pathogenesis and (ii) identifying potential heme/iron-related targets for antifungal therapy. Initially, we validated the behavior of the heme sensor by demonstrating responsiveness to exogenous hemin by established microscopic, fluorimetric, and flow cytometry methods (41). Importantly, we demonstrated that the sensor detected the reduction in cytosolic heme levels expected to result from impaired endocytosis. Specifically, reduced cytosolic heme levels were found in cells treated with CPZ and in mutants such as the cig1 and las17 mutants that have lower heme ...
TY - JOUR. T1 - Kinetics and localisation of haemin-induced lipoprotein oxidation. AU - Morales, Noppawan Phumala. AU - Chunephisal, Pacharaporn. AU - Janprasit, Jindaporn. AU - Ishida, Yuma. AU - Luechapudiporn, Rataya. AU - Yamada, Ken Ichi. N1 - Funding Information: This work was supported by research Grant Nos. RMU5080058 and RMU5480001 from the Thailand Research Fund (TRF) and the Commission on Higher Education; by the Office of the Higher Education Commission and Mahidol University under the National Research Universities Initiative; by AMED CREST Grant Number JP19gm0910013 (K.Y.); and by JSPS KAKENHI Grant Nos. 18K19405 (K.Y.) and 17H03977 (K.Y.). The authors thank Miss Chalermkhwan Cherlermchoung, Miss Doungporn Wongroganawong, and Mrs. Paveena Yamanont for technical assistance.. PY - 2019/10/3. Y1 - 2019/10/3. N2 - Haemin (iron (III)-protoporphyrin IX) is a degradation product of haemoglobin in circulating erythrocytes. Haemin may play a key oxidising agent for lipoprotein oxidation in ...
Background: Dental technicians (DTs) are exposed to Beryllium (Be) and other substances capable of inducing lung disease. Heme oxygenase -1 (HO-1) play a protective antioxidant role in the lung. The guanine-thymidine (GT) n repeats in the HO-1 promoter determine HO-1 induction level. Short (GT) n repeats (n = ,25; S genotype) is considered as protective since HO-1 is induced more rapidly than in long (GT) n repeats (n = ≥25; L genotype).. Aims To evaluate the correlation of HO-1 polymorphisms to functional and exposure parameters in DTs and the protective role of HO-1 on Be Oxide (BeO) exposed A549 epithelial cells apoptosis.. Methods 65 DTs were followed-up for 2 years by questionnaires,induced sputum (IS) particles size distribution laser analysis (Dapi 2000 Donner Tech and Pulmonary Function Tests. HO-1 genotyping was done by PCR DNA sequencer (AB prism 310). A549 epithelial cell line was cultured with BeO and pretreated with Hemin and Znpp (for stimulation and inhibition of HO-1 ...
What do Snoop Dogg, Jonny Wilkinson and a Buddhist monk all have in prevalent? Why, theyve all completed our exercise diary sequence, which turned a 12 months aged just now. (Just about) each and every 7 days, I have interviewed a large host of persons about one particular factor: how they perform out and what they try to eat about the program of a normal 7 days. We have spoken to Olympians and specialist athletes we have spoken to writers and actors and, of program, the aforementioned spiritual determine, Haemin Sunim. Occasionally we chat far more about self-treatment than calisthenics and from time to time these persons are creatures of extreme schedule when other individuals are all about the spot. It is normally, inevitably, intriguing.. As somebody who also goes to the health and fitness center and seems to be just after himself (or attempts to), but is not a specialist athlete, you could possibly assume that listening to a design clarify how generally they do ab crunches could possibly ...
Good girl.... Gone are the days when I had 5 litre flasks of Harriss haematoxylin ripening in the Stoke-on-Trent sunshine; I felt like an alchemist. Then it was plagiarised Gills haematoxylin ripening, then some infernal lead haematoxylin concoction that turned everything it touched black; I strangely put on weight too. The ripening of haematoxylin to haematin then to oxyhaematin was a delight to witness, the latter meant you have gone too far. The ability to carry out an H&E progressively without having to remove the cytoplasmic overstaining a delight. Im one for keeping home made haematoxylin together with retaining the a in haematin, but on both points alas I feel I shall fail. -----Original Message----- From: Bauer, Karen [mailto:[email protected]] Sent: 01 March 2005 18:02 To: [email protected] Subject: [Histonet] Hematoxylin[Scanned] Hello, I was just wondering what everyone is using for Hematoxylin these days. We are one of those rare Histology Labs that makes ...
Activation of heme oxygenase-1 (HO-1), a heme-degrading enzyme responsive to a wide range of cellular stress, is traditionally considered to convey adaptive responses to oxidative stress, inflammation and vasoconstriction. These diversified effects a
they respond differently from younger subjects. Other reported Reversible renal shutdown has been observed in a case where clinical experience has not identified differences in response an excessive hematin dose (12.2 mg/kg) was administered in between the elderly and younger patients. In general, dose a single infusion. Oliguria and increased nitrogen retention selection for an elderly patient should be cautious, usually occurred although the patient remained asymptomatic.4 No starting at the low end of the dosing range, reflecting the worsening of renal function has been seen with administration greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy ...
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... üzvlerine de nezer salsaq hemin hadiseni izleye bilerik: ekseriyyet diline güc verir, hamı danışanda merddir, cesaret dağıdır ...
Musique en Chemin - 70 km. - Festival Eclats de Voix in Auch - 40 km. - Festival Welcome in Tziganie in Auch - 40 km ...
Hae Min Lee says shes "disgusted" by police over photo of her missing daughter ...
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  • Before starting treatment with hemin, your doctor will test you for the presence of an acute porphyria attack. (
  • Before you start treatment with hemin, your doctor may perform tests to make sure you are having an actual porphyria attack. (
  • Moreover, cell treatment with hemin, a natural source of CO, resulted in comparable VLA-4 ligand dissociation. (
  • Conclusions: Elevation in circulating hepatic ALAS1 and response to treatment with hemin indicate that the liver is an important source of excess ALA in ADP, although the marrow may also contribute. (
  • Hemin is a heme-oxygenase inducer, which can confer anti-inflammatory, cytoprotective, and antiapoptotic effects. (
  • Here, we assessed heme oxygenase-1 (HO-1), which is a crucial antioxidative, antiapoptotic molecule against intracellular stresses, for its therapeutic potential via its inducer, hemin. (
  • To measure NO production, inducible NO synthase (iNOS), HO-1 expression and mitogen-activated protein (MAP) kinase activation we used hemin as an HO-1 inducer and tin protoporphyrin (SnPP) IX as an inhibitor of HO-1 activity in human astrocyte cultures prior to IL-1β exposure. (
  • In this study, we administered hemin (ferriprotoporphyrin chloride, 30 μmol/kg b.w., subcutaneously), a potent inducer of HO-1, every 3 days to rats following subcutaneous administration of MCT (60 mg/kg) and examined its effect on MCT-induced PH and pulmonary inflammation. (
  • In this study, the HO inducer, hemin, lowered blood pressure and attenuated cardiac/renal hypertrophy, whereas the HO inhibitor, chromium mesoporphyrin (CrMP), nullified the effects of hemin and exacerbated cardiac/renal injury the DOCA-salt hypertensive rats. (
  • In conclusion, haemin is a potent inducer of lipoprotein oxidation, and the target site for this oxidation is near the hydrophobic core of the lipoprotein leading to the loss of antioxidant activities and changes in lipid composition and physical properties. (
  • A lyophilised form of hemin is used as a pharmacological agent in certain cases for the treatment of porphyria attacks, particularly in acute intermittent porphyria. (
  • Hemin injection is used to reduce the repeated attacks of porphyria (blood disorder) in some women during their menstrual periods after other treatments (eg, carbohydrate therapy) did not work. (
  • Hemin is used to treat the symptoms of occasional attacks of porphyria related to the menstrual cycle in women. (
  • Hemin should not be used to treat porphyria that affects the skin, also called porphyria cutanea tarda. (
  • Hemin is not a cure for porphyria. (
  • Hemin is usually given after other medicines to treat porphyria have been given for a certain amount of time. (
  • Hemin is produced from red blood cells and is approved by the Food and Drug Administration for treating acute porphyria, which is an inherited condition caused by an enzyme deficiency. (
  • HEMIN (HEE min) is used to treat some forms of a hereditary condition known as acute intermittent porphyria. (
  • How should haem arginate (human hemin) be administered in the management of acute porphyria? (
  • These findings suggest an important role of hemin-induced HO-1 activity as a host defense mechanism against HIV-1 infection. (
  • The present study investigated the role of hemin-induced HO-1 as a putative protection factor against HIV infection. (
  • The role of hemin or HO-1 in the pancreas and their potential modulation of pancreatic injury are unknown. (
  • In this study we wanted to determine the role of hemin and various growth media on the fluorescing properties of S. mutans under planktonic (total biomass) and biofilm (biofilm mass) growth conditions. (
  • The role of hemin and porphyrin-related compounds in the metabolism of S. mutans should be elucidated. (
  • Recently, researchers have witnessed major advances in our understanding of the physiological role of hemin. (
  • What are the possible side effects of hemin? (
  • In order to evaluate potential treatment therapies, we studied the effects of hemin on neurotoxicity of neonatal rat sevoflurane exposure. (
  • Tell your doctor if you have ever had any unusual or allergic reaction to hemin or any other medicines. (
  • Hemin is protoporphyrin IX containing a ferric iron (Fe3+) ion with a coordinating chloride ligand. (
  • The iron ion in haem is ferrous (Fe2+), whereas it is ferric (Fe3+) in both hemin and hematin. (
  • The key difference between heme and hemin is that heme contains ferrous ion, whereas hemin contains ferric ion . (
  • Hemin is a type of porphyrin containing chlorine, and it can form from heme groups, including heme B. This compounds' structure is named protoporphyrin IX, and it contains a ferric iron ion containing a coordinating chloride ligand. (
  • Heme is a biochemical substance that is necessary to bind oxygen in the bloodstream while hemin is a type of porphyrin containing chlorine that can form from heme group, including heme B. The key difference between heme and hemin is that heme contains ferrous ion, whereas hemin contains ferric ion. (
  • Overexpression of the ferric uptake regulator (fur) represses transcription of tonB in the presence of excess hemin, whereas overexpression of the rhizobial iron regulator (rirA) has no effect on hut locus transcription. (
  • hemin or ferric ammonium citrate). (
  • Ten of these, including hemin-utilization genes, have a promoter with a putative ferric-uptake regulator (Fur) binding site. (
  • However, the presence of excess hemin or iron reversed this dominance. (
  • Previous reports showed that the administration of HO inducers like hemin or SnCl 2 for 4 consecutive days restored blood pressure (BP) to the physiological level in young (8 weeks) but not in adult spontaneously hypertensive rats (SHRs). (
  • Administration of hemin can reduce heme deficits in such patients, thereby suppressing the activity of delta-amino-levulinic acid synthase (a key enzyme in the synthesis of the porphyrins) by biochemical feedback, which in turn reduces the production of porphyrins and of the toxic precursors of heme. (
  • Hemin works by lowering the production of a certain enzyme in the body. (
  • Suppression of HIV replication in hemin-activated cells correlated with the induction of HO-1 and was attenuated by tin protoporphyrin (SnPP) IX, an inhibitor of HO-1 activity, suggesting a pivotal role of this endogenous enzyme in the regulation of HIV infection. (
  • Hemin upregulates heme oxygenase-1 (HO-1), a stress-induced enzyme implicated in protection from a variety of injuries while its related isoform HO-2 is constitutively expressed. (
  • A simple, enzyme-free supersandwich-type biosensor is fabricated for the ultrasensitive detection of microRNAs (miRNAs) using N-doped graphene/Au nanoparticles (NG-AuNPs) and hemin/G-quadruplexes. (
  • Given the great benefits of artificial enzymes, a simple approach is proposed via assembling of Ni 2+ with hemin for synthesis of Ni-hemin metal-organic-frameworks (Ni-hemin MOFs) mimic enzyme. (
  • Trypsin-like enzyme activity of whole cultures was also greater at each growth rate under haemin-excess conditions while, conversely, collagenolytic activity was generally higher in haemin-limited cultures. (
  • Thus, although growth rate had an effect on the virulence and enzyme activity of P. gingivalis , the availability of haemin for growth was the most significant factor. (
  • and a hemin degradation/storage enzyme, HemS. (
  • EC, and (b) hemin prevents this conversion by blocking the interaction of cyclic AMP with the kinase's regulation subunit, thereby rendering the enzyme inactive. (
  • Mel activates astrocytes through PKCα/Nrf2/HO-1 signaling pathway to acquire resistance to toxicity of hemin and resist from oxidative stress and apoptosis. (
  • In mouse studies, hemin, a biological product of red blood cells, has been shown to boost the production of HO-1, thereby reducing oxidative stress, allowing repair of the ICC network and normalizing gastric function. (
  • When pretreated with SnPP, the inhibitory effect of hemin on IL-1β-induced NO production and iNOS expression was reversed, suggesting the involvement of HO-1. (
  • The inhibitory effect of hemin was not dependent on the dietary fat level, and no association could be established between colonic carcinogenesis and the lipid oxidation rate measured as fecal TBARS. (
  • Several proteins in human blood bind to hemin, such as hemopexin and serum albumin. (
  • It is very important that your doctor check your progress at regular visits to make sure hemin is working properly. (
  • The inhibition of heme oxygenase system or GSH synthesis with tin mesoporphyrin and buthionine sulfoximine, respectively, suppressed the protective effect of curcumin against hemin-induced toxicity. (
  • We have studied the effect of hemin on reactive oxygen species synthesis, and mild mitochondrial uncoupling in isolated rat brain mitochondria. (
  • Hans Fischer (27 July 1881 - 31 March 1945) was a German organic chemist and the recipient of the 1930 Nobel Prize for Chemistry 'for his researches into the constitution of haemin and chlorophyll and especially for his synthesis of haemin. (
  • In both cell lines, deletion of the hemin-binding octapeptide repeat domain inhibited PrP C -mediated increases in hemoglobin synthesis and PrP C internalization. (
  • Pharmaceutical inhibition of PrP C -hemin elicited increases in hemoglobin synthesis and also limited the propagation of pathological PrP sc , for example in CJD. (
  • Collectively, these results implicate PrP C in promoting neuronal survival in physiological conditions and in cerebral hemorrhage by clearing hemin from the neuronal microenvironment and upregulating the synthesis of hemoglobin. (
  • Tripathi AK, Singh N. Prion Protein-Hemin Interaction Upregulates Hemoglobin Synthesis: Implications for Cerebral Hemorrhage and Sporadic Creutzfeldt-Jakob Disease. (
  • Isolation and characterization of a hemin-binding cell envelope protein from Porphyromonas gingivalis. (
  • A 30 kDa (heated 24 kDa) hemin-binding protein whose expression is both hemin and iron regulated was identified and purified in Porphyromonas gingivalis 381. (
  • N-terminal amino acid sequence analysis of CNBr-digested 24 kDa hemin binding protein revealed that this protein belongs to a new, so far undescribed hemin-binding class of proteins. (
  • We found that multiple monomeric hemin cofactors can be efficiently loaded into the protein nanocage. (
  • Treatment of monocytes with hemin substantially inhibited HIV replication, as evident by nearly undetectable viral RNA and cell-free HIV-1 p24 protein in a dose-dependent manner. (
  • Intraperitoneal hemin administration dramatically increases peritoneal and pancreas macrophages that overexpress HO-1 in association with pancreatic induction of the chemoattractants monocyte chemotactic protein-1 and macrophage inflammatory protein-1α but not RANTES or macrophage inflammatory protein-2. (
  • We determined that eight membrane-associated proteins from B. quintana bind hemin and that a ∼25-kDa protein (HbpA) was the dominant hemin-binding protein. (
  • Transport of haemin across the cytoplasmic membrane through a haemin-specific periplasmic binding-protein-dependent transport system in Yersinia en. (
  • The Yersinia enterocolitica O:8 periplasmic binding-protein-dependent transport (PBT) system for haemin was cloned and characterized. (
  • It consisted of four proteins: the periplasmic haemin-binding protein HemT, the haemin permease protein HemU, the ATP-binding hydrophilic protein HemV and the putative haemin-degrading protein HemS. (
  • As Escherichia coli strains expressing only the haemin outer membrane receptor protein HemR from Y. enterocolitica were capable of using haemin as an iron source the existence of an E. coli K-12 haemin-specific PBT system is postulated. (
  • The first gene in the Y. enterocolitica haemin-specific PBT system encoded a protein, HemS, which is probably involved in the degradation of haemin in the cytoplasm. (
  • Pretreatment with hemin alone substantially induced both HO-1 mRNA and protein expression, and HO-1 mRNA expression was further enhanced when hemin was combined with IL-1β treatment. (
  • Below are the list of possible Hemin transport system permease protein products. (
  • The interaction of prion protein and hemin, a therapeutic opportunity for Creutzfeldt-Jakob disease and cerebral hemorrhage? (
  • Induction was concentration dependent and time dependent, with maximal (about 4-fold) increases in neuroglobin mRNA and protein levels occurring with 50 μM hemin and at 8 to 24 hours. (
  • The inductive effect of hemin was attenuated by the protein kinase G inhibitor KT5823 and the soluble guanylate cyclase inhibitor LY83583, was mimicked by treatment with 8-bromo-cyclic guanosine 3′,5′-monophosphate, and was accompanied by a greater than 10-fold increase in cGMP levels, suggesting that it is mediated through protein kinase G and soluble guanylate cyclase. (
  • In contrast, hypoxic induction of neuroglobin was blocked by the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor PD98059, indicating that hemin and hypoxia regulate neuroglobin expression by different mechanisms. (
  • Heme and hemin are porphyrin protein molecules. (
  • 1] "The hmu locus of Yersinia pestis is essential for utilization of free haemin and haem-protein complexes as iron sources. (
  • Ochoa, S. (1978) Translational control by hemin is due to binding to cyclic AMP-dependent protein kinase Proceedings of the National Academy of Sciences of the United States of America, 75 (3). (
  • This suggests that cyclic AMP and hemin bind to different sites on the protein and that hemin binding affects cyclic AMP binding in an allosteric manner. (
  • Forty-five protein spots that represented thirty-four genes were newly identified in this study, including iron -containing proteins and hemin -containg proteins such as fumarate reductase , iron -sufur subunit(FrdB), ribonucleoside diphosphate reductase , beta subunit (NrdB), glutamyl- tRNA reductase (HemA), nikel- cobalt -cadnium resistance protein (NccB), and porphobilinogen deaminase (HemC). (
  • Hemin inhibits the large conductance potassium channel in brain mitochondria: a putative novel mechanism of neurodegeneration. (
  • Call your doctor for instructions if you miss a dose of hemin. (
  • Male CD-1 mice with TNBS-induced colitis were treated with a daily dose of hemin 5 mg/kg body weight/day and 10 mg/kg body weight/day intraperitoneal, during 4 days. (
  • Taken together, our data show that hemin inhibits mitoBKCa and partially abolishes some of the cytoprotective properties of potassium channel opening. (
  • We now show that hemin blocks cyclic AMP binding because it itself binds specifically to the regulatory subunit. (
  • The protective effect of hemin fails to occur if cells have been preincubated with this agent for 72 h before they are exposed to Adriamycin in the absence of hemin. (
  • various growth media (TSB, BHI, THB) and the presence/absence of hemin and interactions among the factors. (
  • To improve the solubility and in vivo pharmacokinetics of hemin for clinical applications, we developed a micellar hemin by conjugating it with poly(ethylene glycol) (PEG) (PEG-hemin). (
  • Hence, developing a simple method to improve the solubility of hemin is still a major challenge. (
  • A. The experiment involved sequential addition of the fluorescent LDV-FITC probe (25 nM), and different concentrations of hemin (6-100 μM) or DMSO (vehicle). (
  • Tra nsmission electron microscopic images showed that hemin nanoparticles with different initial concentrations of hemin (0.1 and 0.5 mg/mL) were tadpole-shaped (head of approximately 200 nm and tail of 100 nm) and sphere-shaped (50-100 nm), respectively. (
  • Prior research has emphasized the therapeutic potential of hemoproteins as potential drug targets for CJD, which led Singh and Tripathi to explore the interaction between hemin and PrP c in their most recent study. (
  • An acid-base interaction between hemin and PAMAM dendrimers affords supramolecular non-covalent peroxidase systems whose catalytic activity is enhanced after spontaneous electrostatic self-assembling onto a solid surface. (
  • Experiments were performed with K562 erythroleukemia cells to further characterize the observation that hemin protects hemopoietic cells from the cytotoxic effects of anthracycline drugs. (
  • Exposure of K562 cells to hemin retards the anthracycline-induced arrest of cells at the G 2 -M interphase of the cell cycle and permits cells to undergo continuing division as demonstrated by clonal growth in plasma clot cultures. (
  • Utilizing fluorescent labelled PrP C , the interaction between PrP C and hemin was investigated in neuroblastoma (SH-SY5Y) and hematopoietic (K562) cell cultures. (
  • Acquisition of heat shock factor 2 (HSF2) DNA binding activity is accompanied by induced transcription of heat shock genes in hemin-treated K562 cells undergoing erythroid differentiation. (
  • We show that in parental K562 cells, the HSF2-alpha isoform is predominantly expressed and HSF2 can be activated upon hemin treatment. (
  • We suggest that HSF2-beta acts as a negative regulator of HSF2 activity during hemin-mediated erythroid differentiation of K562 cells. (
  • Hence, in this study, we examined the effects of AHSP knockdown in hemin-induced K562 and erythropoietin-induced CD34(+) cells with particular reference to cellular aspects and gene expression. (
  • Hemin is a product of hemoglobin degradation, which has strong toxicity and can induce reactive oxygen species (ROS). (
  • Liu, X., Zhang, X., Li, N. Study of a Magnetic Photocatalyst Based on Hemin with Axial Ligand and its Degradation under Visible Light. (
  • Haemin (iron (III)-protoporphyrin IX) is a degradation product of haemoglobin in circulating erythrocytes. (
  • Hemin (ferriprotoporphyrin IX chloride), the oxidized form of the heme moiety of hemoglobin and a constituent of many enzymes, is degraded by heme oxygenase (HO)-1, which in turn generates carbon monoxide (CO), iron and biliverdin. (
  • Hemin-induced HO-1 induction in the CCR-5, CXCR-4, and CD4 coexpressing GHOST(3) cells was consistent with the inhibition of Tat-dependent activation of long terminal repeat promoter leading to reduced GFP expression. (
  • Considering the role of the mitoBKCa in cytoprotection, it can be presumed that its inhibition by hemin may be a novel mechanism contributing to the severity of the ICH symptoms. (
  • Conversely, outcomes in cerebral hemorrhage may be improved by inhibiting hemin-induced endocytosis of PrP C . The downstream effects of such inhibition would preclude the upregulation of hemoglobin and improve neuronal viability by clearing extracellular hemin and increasing respiratory potential. (
  • Datta, K. (1986) Affinity purification and properties of rat liver mitochondrial L-alanine:4,5-dioxovalerate transaminase and its inhibition by hemin Archives of Biochemistry and Biophysics, 248 (2). (
  • Hemin, a critical component of hemoglobin, is an active ingredient of a biologic therapeutic approved by the Food and Drug Administration for the treatment of acute porphyries. (
  • Since the 1970s, when it was approved by the Food and Drug Administration, hemin has been used to successfully treat a variety of disorders, such as acute porphyries, control of liver allograft failure due to recurrence of erythopoietic protophoria, and thalassemia intermedia ( 10 , 11 , 12 ) with minimal side effects. (
  • Therefore, hemin-like compounds or hemin-activated macrophages may offer novel therapeutic approaches for preventing acute pancreatitis and its pulmonary complication via upregulation of HO-1. (
  • Intravenous hemin was effective in most reported cases for treatment and prevention of acute attacks of neurological symptoms. (
  • 1) group C: non-anesthesia, (2) group H: intraperitoneal hemin (50 mg kg-1) treatment on days 5 and 6, (3) group S: 3% sevoflurane exposure for 4 h, and (4) group SH: hemin treatment + sevoflurane exposure. (
  • Such pharmacological forms of hemin are sold under a range of trade names including the trademarks Panhematin and Normosang. (
  • C. The experiment was conducted using U937 cells stably transfected with the FPR ΔST receptor, and involved sequential addition of the fluorescent LDV-FITC probe (4 nM), the high affinity FPR ligand N-formyl-Met-Leu-Phe-Phe (100 nM), hemin (1.5-100 μM) or DMSO (control), and LDV (2 μM). (
  • An investigation was conducted on hemin modified with axial ligand loaded onto magnetic carriers which created a kind of visible-light activated photocatalyst with good magnetic property. (
  • PEG-hemin showed higher solubility in water and significantly prolonged plasma half-life than free hemin, which resulted from its micellar nature with molecular mass of 126 kDa in aqueous media. (
  • Moreover, hemin nanoparticles exhibited higher solubility than free hemin. (
  • We postulated that the solubility of hemin nanoparticles could be increased compared to free hemin, which could have valuable applications. (
  • Normosang injection contains human hemin, which is a substance derived from human blood. (
  • Human hemin injection is given to supplement the body with haem. (
  • In this study subjects were randomized to intravenous hemin, prepared in albumin, or albumin alone. (
  • Now, Dr. Farrugia and colleague Adil E. Bharucha, MBBS, M.D., are recruiting patients for the first randomized controlled clinical trial to determine whether intravenous hemin therapy is equally beneficial for people with gastroparesis. (
  • We further show that extracellular hemin concentration correlates closely with changes in RBC deformability and we confirm that this biophysical change correlates with other indicators of cell stress. (
  • These data suggest that the pretreatment with curcumin induces Nrf2 and an antioxidant response that may play an important role in the protective effect of this antioxidant against hemin-induced neuronal death. (
  • Hemin reduced neuronal apoptosis, improved mitochondrial dynamics and protected against cognitive deficits induced by sevoflurane in neonatal rats. (
  • Detection and comparison of specific hemin binding by Porphyromonas gingivalis and Prevotella intermedia. (
  • Porphyromonas gingivalis strain W50 was grown under haemin-limitation and haemin-excess conditions in a chemostat at pH 7·5. (
  • In order to do so, we have used a patch-clamp technique and shown that hemin inhibits mitoBKCa in human astrocytoma U-87 MG cell line mitochondria. (
  • Hemin can be produced from hemoglobin by the so-called Teichmann test, when hemoglobin is heated with glacial acetic acid (saturated with saline). (
  • The hemin-treated mice presented a decrease in fecal hemoglobin, ALP, and proinflammatory cytokine concentrations compared to the TNBS group. (
  • Neena Singh and Ajai Tripathi's recent research from Case Western Reserve University School of Medicine (OH, USA) may offer exciting new insights into prion protein's (PrP) binding motif and its interactions with hemin, a toxic byproduct of hemoglobin. (
  • Here we report that, like hemoglobin and myoglobin, neuroglobin expression can also be induced by hemin. (
  • We propose a model of haemin utilization in Y. enterocolitica in which HemT, HemU and HemV proteins transport haemin into the cytoplasm where it is degraded by HemS thereby liberating the iron. (
  • To upregulate the expression of heme oxygenase (HO) to lower blood pressure (BP) of spontaneously hypertensive rats (SHRs), we administered hemin to 12-week-old adult SHRs through subcutaneously implanted osmotic minipumps for 3 consecutive weeks (the hemin protocol). (
  • This study identifies curcumin as a neuroprotectant against hemin-induced damage in primary cultures of cerebellar granule neurons (CGNs) of rats. (
  • The present study has been designed to investigate the combined effect of daidzein (caveolin inhibitor), hemin (hemoxygenase activator) and BMS182874 (endothelin receptor antagonist) in diabetic nephropathy in wistar rats. (
  • L-NAME (NG-nitro- L-arginine methyl ester) a selective eNOS inhibitor abolished the ameliorative effect of combination of daidzein, hemin and BMS182874 in DN in rats. (
  • The Neuroprotective Effect of Hemin and the Related Mechanism in Sevoflurane Exposed Neonatal Rats. (
  • Only hemin among the intermediate compounds of heme metabolism tested was shown to be an inhibitor of purified alanine:4,5-dioxovalerate transaminase. (
  • Hemin was further shown as an uncompetitive inhibitor of both alanine and dioxovalerate. (
  • Spontaneous mutation to a Pgm- phenotype results in the loss of a number of divergent physiological characteristics, including the ability to store hemin and to bind Congo red at 26 degrees C. In this study, we generated and isolated transposon insertion mutants that are hemin storage negative (Hms-) and therefore unable to form pigmented colonies. (
  • Liu J, Xin XY, Zhou H, Zhang SS (2015) A ternary composite based on graphene, hemin, and gold nanorods with high catalytic activity for the detection of cell-surface glycan expression. (
  • The reduced graphene oxide-hemin-cysteine (rGO-H-Cys) composite and Au-PtNWs acted not only as amplification labels to amplify signals via synergetic catalysis, but also as an ideal nanocarrier to accelerate electron transfer. (
  • Herein, we reported a simple colorimetric strategy for label-free quantification of human telomerase activity in urine by using hemin-graphene nanomaterial (H-GNs). (
  • The presence of the hemS gene was necessary to prevent haemin toxicity in E. coli strains that accumulate large amounts of haemin in the cytoplasm. (
  • The upregulation of HO-1 induced by Mel was depressed by knocking down Nrf2 expression by siRNA, which also decreased the resistance of astrocytes to toxicity of hemin. (
  • You should not use hemin if you are allergic to it. (
  • You should not receive it if you had an allergic reaction to hemin. (
  • The present studies demonstrate that this protective effect of hemin applies only to anthracyclines and not to other classes of antineoplastic agents. (
  • The protective effect of hemin was associated with increased HO-1, HO activity, cyclic guanosine monophosphate (cGMP), superoxide dismutase activity, ferritin and the total antioxidant capacity in the cardiac and renal tissue. (
  • ZnPP also inhibited the protective effect of hemin in IL-1beta-treated islets. (
  • Chemically, hemin differs from the related heme-compound hematin chiefly in that the coordinating ion is a chloride ion in hemin, whereas the coordinating ion is a hydroxide ion in hematin. (
  • In chemical terms, the hemin molecule is different from heme-compound hematin because of the chloride ion in hemin in the place of the coordinating hydroxide ion in hematin. (
  • These findings suggest that hemin treatment ameliorates MCT-induced PH possibly mediated through induction of pulmonary HO-1 which leads to the attenuation of pulmonary inflammation. (
  • research into the constitution of hemin, the red blood pigment, and chlorophyll, the green pigment in plants. (
  • Fischer H. "On hemin and the relationships between hemin and chlorophyll" (PDF). (
  • In addition, hemin treatment significantly suppressed infection of both monocytes and T cells inoculated with R5, X4, R5X4 tropic strains, and reverse transcriptase-resistant, azidothymidine-resistant, ddC/ddI-resistant, nivirapine-resistant, and other clinical HIV isolates. (
  • In a rat I/R model, administration of PEG-hemin significantly elevated HO-1 expression and enzymatic activity. (
  • Dietary hemin significantly reduced colonic carcinogenesis. (
  • In contrast, hemin treatment of MCT-administered animals, which led to a further increase in pulmonary HO-1 mRNA expression, significantly ameliorated MCT-induced PH as well as tissue inflammation. (
  • The data showed that the fastest growing cells were significantly more virulent than those grown more slowly, irrespective of haemin concentration. (
  • Oxygen quenching agents in media such as hemin and charcoal as well as a microaerobic atmosphere and preenrichment can significantly improve recovery (2,14-16,21,25,28). (
  • Subinhibitory concentrations of haemin were found to significantly reduce transcription of the haemolysin genes hlb (encoding β-haemolysin) and hlgA (encoding the S-class component of γ-haemolysin), while hla (encoding α-haemolysin) and RNAIII (encoding δ-haemolysin) transcription did not appear to be affected. (
  • The aim of this study is to evaluate the effect of hemin in the 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model. (
  • Sustained upregulation of HO-1-linked signaling pathways and reversal of vascular remodeling in peripheral blood vessels mediate likely the antihypertensive effect of the hemin protocol. (
  • 9 It was perceived that an even longer hemin treatment period might normalize BP and may have a long-lasting effect in SHR with established hypertension. (
  • Multiple underlying mechanisms were investigated to determine the long-lasting antihypertension effect of the hemin protocol. (
  • These results suggest that PEG-hemin exerted a significant cytoprotective effect against I/R injury in rat liver by inducing HO-1 and thus seems to be a potential therapeutic for ROS-related diseases, including I/R injury. (
  • Effect of hemin on binding and dissociation of the LDV-FITC probe on resting and activated U937 cells. (
  • Peroxidase-mimic Ni-hemin MOFs as reactive oxygen species which could damage MCF-7 cancer cells, however for normal cells (human embryonic kidney HEK 293 cells) killing effect was negligible. (
  • Bombicini RL, Schmitt TH, Frezzati Junior WA, Schreier S. Effect of hemin upon structure, permeability and peroxidation of membranes. (
  • Zen teacher Haemin Sunim describes with great clarity the suffocating effect of perfectionism - how damaging it is to think your worth as a person is solely dependent on how you perform. (
  • Inactivation of the sae locus in LS1 abolished the haemin effect on the transcription of haemolysin genes, indicating that the two-component regulatory system is required for this regulatory effect. (
  • 6 ] indicated that crystalline hemin and L-arginate could prepare water-soluble hemin-arginate coacervation, which could be used as a new heme iron supplement in food additives, functional foods, and pharmaceuticals. (
  • Engaged in the research and development of biological products with animal and vegetable as main materials, we now have successfully developed a series of products such as Soybean Extract Cu/Zn-Superoxide Dismutase (SOD), Heme Iron, Hemin, Thrombin, Bilirubin and Food grade plasma Albumen powder, etc. (
  • In contrast, when HSF2-beta is expressed at levels exceeding those of endogenous HSF2-alpha, the hemin-induced DNA binding activity and transcription of heat shock genes are repressed, whereas overexpression of HSF2-alpha results in an enhanced hemin response. (
  • Identification and cloning of a hemin storage locus involved in the pigmentation phenotype of Yersinia pestis. (
  • Restriction site analysis of eight mutants identified a minimum of six potentially different insertion sites spanning an approximately 10-kb hemin storage (hms) locus. (
  • mini-kan mutations and cloned wild-type hms locus generated in this study will greatly aid in identifying the function of hemin storage in Y. pestis. (
  • Irr functions as a transcriptional repressor of the hut locus at all hemin concentrations tested. (
  • Y. enterocolitica strains mutated in hemU or hemV genes were unable to use haemin as an iron source whereas those mutated in the hemT gene were able to use haemin as an iron source. (
  • These effects may be mediated by direct interactions of hemin with DNA and perhaps other cellular constituents or by molecular complex formation between hemin and anthracyclines at intracellular sites. (
  • These findings suggest that hemin treatment reduces hemorrhagic focus, intestinal damage, tissue inflammation, and lesion extension associated with experimental colitis. (
  • The findings from this study demonstrate that hemin-mediated augmentation of HO-1 activity substantially suppresses HIV replication both in vitro and in vivo with no apparent toxic effects. (
  • The findings suggest that hemin prevents anthracycline-induced cytotoxicity by acting at several levels. (
  • In such pharmacological contexts, hemin is typically formulated with human albumin prior to administration by a medical professional, to reduce the risk of phlebitis and to stabilize the compound, which is potentially reactive if allowed to circulate in free-form. (
  • Hemin, the oxidized form of heme, is a highly reactive compound that induces cellular injury. (
  • Moreover, 15 μ M curcumin attenuated by 55% the increase in reactive oxygen species (ROS) production, by 94% the reduction of GSH/glutathione disulfide (GSSG) ratio, and by 49% the cell death induced by hemin. (
  • The mechanism for the decomposition of the LbL film was considered to involve a more reactive oxygen species (ROS) that was formed by the reaction of hemin and H2O2, which then caused nonspecific DNA cleavage. (
  • Bartonella quintana , the agent of trench fever and a cause of endocarditis and bacillary angiomatosis in humans, has the highest reported in vitro hemin requirement for any bacterium. (
  • In a recent study hemin was used to induce HO-1 in humans [ 4 ]. (
  • Hemin injection may increase iron levels in the blood. (
  • In mice with diabetes and slow gastric emptying, hemin increases HO-1 activity and improves gastric emptying. (
  • Hemin administration before CDD feeding protected 8 of 8 mice from lethality while 7 of 16 controls died. (
  • Protection is mediated by HO-1-overexpressing macrophages since hemin-primed macrophages home to the pancreas after transfer to naive mice and protect from CDD-induced pancreatitis. (

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