Buthionine Sulfoximine: 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)Methionine SulfoximineGlutathione: 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.Glutamate-Cysteine Ligase: 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 6.3.2.2.MaleatesAntimetabolites: Drugs that are chemically similar to naturally occurring metabolites, but differ enough to interfere with normal metabolic pathways. (From AMA Drug Evaluations Annual, 1994, p2033)Acetylcysteine: The N-acetyl derivative of CYSTEINE. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates.Glutathione Synthase: One of the enzymes active in the gamma-glutamyl cycle. It catalyzes the synthesis of glutathione from gamma-glutamylcysteine and glycine in the presence of ATP with the formation of ADP and orthophosphate. EC 6.3.2.3.Glutathione Disulfide: A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.Cystine: A covalently linked dimeric nonessential amino acid formed by the oxidation of CYSTEINE. Two molecules of cysteine are joined together by a disulfide bridge to form cystine.Oxidative Stress: 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).Pyrrolidonecarboxylic Acid: A cyclized derivative of L-GLUTAMIC ACID. Elevated blood levels may be associated with problems of GLUTAMINE or GLUTATHIONE metabolism.Glutathione Reductase: Catalyzes the oxidation of GLUTATHIONE to GLUTATHIONE DISULFIDE in the presence of NADP+. Deficiency in the enzyme is associated with HEMOLYTIC ANEMIA. Formerly listed as EC 1.6.4.2.Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).Drug Resistance: Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.Diamide: A sulfhydryl reagent which oxidizes sulfhydryl groups to the disulfide form. It is a radiation-sensitizing agent of anoxic bacterial and mammalian cells.Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.Sulfhydryl Compounds: Compounds containing the -SH radical.Antioxidants: 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.Reactive Oxygen Species: Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.gamma-Glutamyltransferase: An enzyme, sometimes called GGT, with a key role in the synthesis and degradation of GLUTATHIONE; (GSH, a tripeptide that protects cells from many toxins). It catalyzes the transfer of the gamma-glutamyl moiety to an acceptor amino acid.Hydrogen Peroxide: 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.Glutathione Peroxidase: An enzyme catalyzing the oxidation of 2 moles of glutathione in the presence of hydrogen peroxide to yield oxidized glutathione and water. EC 1.11.1.9.Drug Synergism: The action of a drug in promoting or enhancing the effectiveness of another drug.Oxidants: Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Arsenicals: Inorganic or organic compounds that contain arsenic.Glutathione Transferase: A transferase that catalyzes the addition of aliphatic, aromatic, or heterocyclic FREE RADICALS as well as EPOXIDES and arene oxides to GLUTATHIONE. Addition takes place at the SULFUR. It also catalyzes the reduction of polyol nitrate by glutathione to polyol and nitrite.Glutamate-Ammonia Ligase: An enzyme that catalyzes the conversion of ATP, L-glutamate, and NH3 to ADP, orthophosphate, and L-glutamine. It also acts more slowly on 4-methylene-L-glutamate. (From Enzyme Nomenclature, 1992) EC 6.3.1.2.Antimetabolites, Antineoplastic: Antimetabolites that are useful in cancer chemotherapy.Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Cysteine: A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.Catalase: An oxidoreductase that catalyzes the conversion of HYDROGEN PEROXIDE to water and oxygen. It is present in many animal cells. A deficiency of this enzyme results in ACATALASIA.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.Libraries, NursingDrug-Induced Liver Injury: A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, and chemicals from the environment.Analgesics, Non-Narcotic: A subclass of analgesic agents that typically do not bind to OPIOID RECEPTORS and are not addictive. Many non-narcotic analgesics are offered as NONPRESCRIPTION DRUGS.Gold Sodium Thiomalate: A variable mixture of the mono- and disodium salts of gold thiomalic acid used mainly for its anti-inflammatory action in the treatment of rheumatoid arthritis. It is most effective in active progressive rheumatoid arthritis and of little or no value in the presence of extensive deformities or in the treatment of other forms of arthritis.Nitrosation: Conversion into nitroso compounds. An example is the reaction of nitrites with amino compounds to form carcinogenic N-nitrosamines.Prostatic Hyperplasia: Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.Reactive Nitrogen Species: Nitrogenous products of NITRIC OXIDE synthases, ranging from NITRIC OXIDE to NITRATES. These reactive nitrogen intermediates also include the inorganic PEROXYNITROUS ACID and the organic S-NITROSOTHIOLS.Robotics: The application of electronic, computerized control systems to mechanical devices designed to perform human functions. Formerly restricted to industry, but nowadays applied to artificial organs controlled by bionic (bioelectronic) devices, like automated insulin pumps and other prostheses.Patents as Topic: Exclusive legal rights or privileges applied to inventions, plants, etc.Chlormadinone Acetate: An orally active synthetic progestational hormone used often in combinations as an oral contraceptive.DNA Topoisomerases, Type I: DNA TOPOISOMERASES that catalyze ATP-independent breakage of one of the two strands of DNA, passage of the unbroken strand through the break, and rejoining of the broken strand. DNA Topoisomerases, Type I enzymes reduce the topological stress in the DNA structure by relaxing the superhelical turns and knotted rings in the DNA helix.Topoisomerase I Inhibitors: Compounds that inhibit the activity of DNA TOPOISOMERASE I.Camptothecin: An alkaloid isolated from the stem wood of the Chinese tree, Camptotheca acuminata. This compound selectively inhibits the nuclear enzyme DNA TOPOISOMERASES, TYPE I. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity.Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.

Influence of glutathione levels and heat-shock on the steady-state levels of oxidative DNA base modifications in mammalian cells. (1/573)

The effects of thiols, ascorbic acid and thermal stress on the basal (steady-state) levels of oxidative DNA base modifications were studied. In various types of untreated cultured mammalian cells, the levels of total glutathione were found to be inversely correlated with the levels of DNA base modifications sensitive to the repair endonuclease Fpg protein, which include 8-hydroxyguanine (8-oxoG). A depletion of glutathione by treatment with buthionine sulphoximine increased the steady-state level in AS52 Chinese hamster cells by approximately 50%. However, additional thiols in the culture medium did not reduce the level of Fpg-sensitive base modifications: 0-10 mM N-acetylcysteine had no effect, whereas cysteine ethylester even increased the oxidative DNA damage at concentrations >0.1 mM. Similarly, ascorbic acid (0-20 mM) failed to reduce the steady-state levels. When AS52 cells were grown at elevated temperature (41 degrees C), the steady-state level of the oxidative DNA modifications increased by 40%, in spite of a concomitant 1.6-fold increase of the cellular level of total glutathione. Depletion of glutathione at 41 degrees C nearly doubled the already elevated level of oxidative damage. A constitutive expression of the heat-shock protein Hsp27 in L929 mouse fibrosarcoma cells at 37 degrees C increased the glutathione level by 60%, but had little effect on the level of oxidative DNA damage.  (+info)

Role of antioxidant defenses against ethanol-induced damage in cultured rat gastric epithelial cells. (2/573)

Reactive oxygen species appears to be involved in the pathogenesis of ethanol-induced gastric mucosal injury in vivo. Because ingested ethanol diffuses into the gastric mucosa, targeting both epithelium and endothelium, in the present study we examined the possible protective effect of antioxidants on ethanol damage in gastric epithelial cells and endothelial cells in vitro. Cytotoxicity by ethanol was quantified by measuring 51Cr release. The effects of impairment of the glutathione redox cycle and of inhibition of cellular catalase were examined. The generation of superoxide was assessed by the reduction in cytochrome c. Ethanol caused a time- and dose-dependent increase in 51Cr release from epithelial cells. Incubation of cells with DL-buthionine-(S,R)-sulfoximine, while reducing glutathione production, dose dependently enhanced ethanol-induced injury. 1,3-Bis(chloroethyl)-nitrosourea, while inhibiting glutathione reductase activity, also sensitized cells to ethanol. In contrast, the inhibition of catalase with 3-amino-1,2, 4-triazole did not alter the susceptibility of epithelial cells to ethanol. Ethanol induced damage to endothelial cells in a similar fashion. In endothelial cells, however, neither impairment of the glutathione cycle nor inhibition of catalase influenced ethanol-induced damage. Epithelial cells, when exposed to ethanol, increased superoxide production as a function of ethanol concentration, whereas endothelial cells did not. The glutathione redox cycle, but not cellular catalase, plays a critical role in protecting epithelial cells against ethanol damage, whereas neither antioxidant seems to play a role in protection of endothelial cells. The distinct difference in antioxidant protection against ethanol appears to depend on the capability of each cell to produce cytotoxic oxygen species in response to ethanol exposure.  (+info)

Involvement of N-acetylcysteine-sensitive pathways in ricin-induced apoptotic cell death in U937 cells. (3/573)

We have found that the antioxidant N-acetylcysteine (NAC) strongly inhibited ricin-induced apoptotic cell death in U937 cells (human myeloid leukemia), as judged by cytotoxicity, nuclear morphological change, and DNA fragmentation. Consistent with these observations, a significant depletion of cellular glutathione was observed in ricin-treated cells, and NAC prevented the decrease in cellular glutathione. On the other hand, among the caspase inhibitors tested, Z-Asp-CH2-DCB, which inhibited ricin cytotoxicity, also suppressed ricin-mediated glutathione depletion, while NAC did not affect the generation of caspase-3 like activity in ricin-treated cells. These results suggest that glutathione loss takes place downstream from caspase activation during the ricin-induced apoptotic process. Treatment with a specific inhibitor of glutathione biosynthesis, buthionine sulfoximine (BSO) failed to induce apoptosis, and had no effect on the overall extent of ricin-induced apoptosis, even though the glutathione level was decreased to less than 5% of the control level. However, NAC still protected against ricin-induced apoptosis in the BSO-treated cells. We conclude that glutathione loss is one of several apoptotic changes caused by ricin, but is not a sufficient factor for the progress of apoptosis. NAC may prevent ricin-induced apoptosis through maintaining an intracellular reducing condition by acting as a thiol supplier.  (+info)

Apoptosis in hematopoietic cells (FL5.12) caused by interleukin-3 withdrawal: relationship to caspase activity and the loss of glutathione. (4/573)

The mechanism of cell death caused by cytokine deprivation remains largely unknown. FL5.12 cells (a murine prolymphocytic cell line), following interleukin-3 (IL-3) withdrawal, undergo a decrease in intracellular glutathione (GSH) that precedes the onset of apoptosis. In the present study, the induction of apoptosis following IL-3 withdrawal or GSH depletion with DL-buthionine-[S,R,]-sulfoximine (BSO) was examined. Both conditions caused time-dependent increases in phosphatidylserine externalization, acridine orange and ethidium bromide staining, decreases in mitochondrial membrane potential, processing and activation of caspase-3 and proteolysis of the endogenous caspase substrate poly(adenosine diphosphate ribose)polymerase (PARP). Apoptosis induced by IL-3 deprivation but not BSO also caused lamin B1 cleavage, suggesting activation of caspase-6. Despite a more profound depletion of GSH after BSO than withdrawal of IL-3, the extent of apoptosis was somewhat lower. Benzyloxycarbonyl-Val-Ala-Asp(OMe)fluoromethyl ketone (z-VAD.fmk) blocked this caspase activity and prevented cell death after BSO exposure but not after IL-3 deprivation. Following IL-3 withdrawal, the caspase inhibitors z-VAD.fmk and boc-asp(OMe)fluoromethylketone (boc-asp.fmk) prevented the cleavage and activation of caspase-3, the breakdown of lamin B1 and partially mitigated PARP degradation. However, the externalization of phosphatidylserine, the fall in mitochondrial membrane potential and subsequent apoptotic cell death still occurred. These results suggest that IL-3 withdrawal may mediate cell death by a mechanism independent of both caspase activation and the accompanying loss of GSH.  (+info)

ATP-Dependent efflux of CPT-11 and SN-38 by the multidrug resistance protein (MRP) and its inhibition by PAK-104P. (5/573)

Non-P-glycoprotein-mediated multidrug-resistant C-A120 cells that overexpressed multidrug resistance protein (MRP) were 10.8- and 29. 6-fold more resistant to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11) and SN-38, respectively, than parental KB-3-1 cells. To see whether MRP is involved in CPT-11 and SN-38 resistance, MRP cDNA was transfected into KB-3-1 cells. The transfectant, KB/MRP, which overexpressed MRP, was resistant to both CPT-11 and SN-38. 2-[4-Diphenylmethyl)-1-piperazinyl]ethyl-5-(trans-4,6-dimethyl-1,3 , 2-dioxaphosphorinan-2-yl)-2, 6-dimethyl-4-(3-nitrophenyl)-3-pyridinecarboxylate P-oxide (PAK-104P) and MK571, which reversed drug resistance in MRP overexpressing multidrug-resistant cells, significantly increased the sensitivity of C-A120 and KB/MRP cells, but not of KB-3-1 cells, to CPT-11 and SN-38. The accumulation of both CPT-11 and SN-38 in C-A120 and KB/MRP cells was lower than that in KB-3-1 cells. The treatment with 10 microM PAK-104P increased the accumulation of CPT-11 and SN-38 in C-A120 and KB/MRP cells to a level similar to that found in KB-3-1 cells. The ATP-dependent efflux of CPT-11 and SN-38 from C-A120 and KB/MRP cells was inhibited by PAK-104P. DNA topoisomerase I expression, activity, and sensitivity to SN-38 were similar in the three cell lines. Furthermore, the conversion of CPT-11 to SN-38 in KB-3-1 and C-A120 cell lines was similar. These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.  (+info)

Protection against hydrogen peroxide cytotoxicity in rat-1 fibroblasts provided by the oncoprotein Bcl-2: maintenance of calcium homoeostasis is secondary to the effect of Bcl-2 on cellular glutathione. (6/573)

The oncoprotein Bcl-2 protects cells against apoptosis, but the exact molecular mechanism that underlies this function has not yet been identified. Studying H2O2-induced cell injury in Rat-1 fibroblast cells, we observed that Bcl-2 had a protective effect against the increase in cytosolic calcium concentration and subsequent cell death. Furthermore, overexpression of Bcl-2 resulted in an alteration of cellular glutathione status: the total amount of cellular glutathione was increased by about 60% and the redox potential of the cellular glutathione pool was maintained in a more reduced state during H2O2 exposure compared with non-Bcl-2-expressing controls. In our cytotoxicity model, disruption of cellular glutathione homoeostasis closely correlated with the pathological elevation of cytosolic calcium concentration. Stabilization of the glutathione pool by Bcl-2, N-acetylcysteine or glucose delayed the cytosolic calcium increase and subsequent cell death, whereas depletion of glutathione by dl-buthionine-(S, R)-sulphoximine, sensitized Bcl-2-transfected cells towards cytosolic calcium increase and cell death. We therefore suggest that the protection exerted by Bcl-2 against H2O2-induced cytosolic calcium elevation and subsequent cell death is secondary to its effect on the cellular glutathione metabolism.  (+info)

Significance of glutathione-dependent antioxidant system in diabetes-induced embryonic malformations. (7/573)

Hyperglycemia-induced embryonic malformations may be due to an increase in radical formation and depletion of intracellular glutathione (GSH) in embryonic tissues. In the past, we have investigated the role of the glutathione-dependent antioxidant system and GSH on diabetes-related embryonic malformations. Embryos from streptozotocin-induced diabetic rats on gestational day 11 showed a significantly higher frequency of embryonic malformations (neural lesions 21.5 vs. 2.8%, P<0.001; nonneural lesions 47.4 vs. 6.4%, P<0.001) and growth retardation than those of normal mothers. The formation of intracellular reactive oxygen species (ROS), estimated by flow cytometry, was increased in isolated embryonic cells of diabetic rats on gestational day 11. The concentration of intracellular GSH in embryonic tissues of diabetic pregnant rats on day 11 was significantly lower than that of normal rats. The activity of y-glutamylcysteine synthetase (gamma-GCS), the rate-limiting GSH synthesizing enzyme, in embryos of diabetic rats was significantly low, associated with reduced expression of gamma-GCS mRNA. Administration of buthionine sulfoxamine (BSO), a specific inhibitor of gamma-GCS, to diabetic rats during the period of maximal teratogenic susceptibility (days 6-11 of gestation) reduced GSH by 46.7% and increased the frequency of neural lesions (62.1 vs. 21.5%, P<0.01) and nonneural lesions (79.3 vs. 47.4%, P<0.01). Administration of GSH ester to diabetic rats restored GSH concentration in the embryos and reduced the formation of ROS, leading to normalization of neural lesions (1.9 vs. 21.5%) and improvement in nonneural lesions (26.7 vs. 47.4%) and growth retardation. Administration of insulin in another group of pregnant rats during the same period resulted in complete normalization of neural lesions (4.3 vs. 21.5%), nonneural lesions (4.3 vs. 47.4%), and growth retardation with the restoration of GSH contents. Our results indicate that GSH depletion and impaired responsiveness of GSH-synthesizing enzyme to oxidative stress during organogenesis may have important roles in the development of embryonic malformations in diabetes.  (+info)

Molecular basis for hepatic detoxifying enzyme induction by 2-(allylthio)pyrazine in rats in comparison with oltipraz: effects on prooxidant production and DNA degradation. (8/573)

The expression of hepatic microsomal epoxide hydrolase (mEH) and glutathione S-transferases (GSTs) by 2-(allylthio)pyrazine (2-AP), an experimental chemopreventive agent, was investigated in rats. Northern blot analysis revealed that 2-AP caused increases in mEH, rGSTA2/3/5, and rGSTM1/2 mRNA levels. mEH and rGSTA2 proteins were also induced. Molecular basis of the enzyme induction by 2-AP was studied in comparison with oltipraz (Olt). Rats exposed to buthionine sulfoximine, a GSH-depleting agent, before treatment with either 2-AP or Olt exhibited greater increases in the mRNA levels than the individual treatment. Conversely, increases of the mRNAs were prevented by cysteine treatment, indicating that metabolic intermediates or reactive oxygens produced from the agents could be reduced by cysteine. Gel shift analysis revealed that nuclear factor-kappaB, which is associated with the altered cellular redox state, was not activated by the agents. Effects of these agents on the breakage of phix-174 DNA were compared in vitro. 2-AP effectively reduced the conversion of supercoiled DNA to the open circular form induced by benzenetriol and prevented benzenetriol- and iron-catalyzed degradation of DNA, whereas Olt failed to prevent strand breakage of DNA. These results provided evidence that: 1) 2-AP was effective in elevating the hepatic mEH and GST gene expression in rats, which might be mediated with the production of reactive oxygen species; 2) nuclear factor-kappaB activation was not involved in the induction of the detoxifying enzymes by either 2-AP or Olt in spite of their production of reactive oxygens in vivo; and 3) the antioxidant effect of 2-AP in vitro differed from that of Olt.  (+info)

*Buthionine sulfoximine

... (BSO) is a sulfoximine which reduces levels of glutathione and is being investigated as an adjunct with ... Buthionine sulfoximine may also be used to increase the sensitivity of parasites to oxidative antiparasitic drugs. Defty, CL; ... "Definition of buthionine sulfoximine - National Cancer Institute Drug Dictionary". ...

*Reactive oxygen species

... buthionine sulfoximine (BSO)). The result is an overall increase in endogenous ROS, which when above a cellular tolerability ...

*Glutamate-cysteine ligase

"Potent and specific inhibition of glutathione synthesis by buthionine sulfoximine (S-n-butyl homocysteine sulfoximine)". J Biol ...

*S-Nitrosoglutathione

... inhibition of iNOS with L-NAME in isolated perfused livers and also in rat livers depleted of GSH with buthionine sulfoximine. ...

*BSO

... and oxygen Buthionine sulfoximine, a chemical substance inhibiting glutathione synthesis Baltimore Symphony Orchestra, Maryland ...

*List of MeSH codes (D12.125)

... methionine sulfoximine MeSH D12.125.166.676.620.125 --- buthionine sulfoximine MeSH D12.125.166.676.900 --- selenomethionine ...

*List of MeSH codes (D02)

... methionine sulfoximine MeSH D02.886.030.676.620.125 --- buthionine sulfoximine MeSH D02.886.030.676.900 --- selenomethionine ...

*Index of oncology articles

... buthionine sulfoximine C cell - c-erbB-2 - c-kit - CA 19-9 assay - CA-125 - CA-125 test - cachexia - calcitonin - calcitriol - ...

*11-Ketoprogesterone

Piwien-Pilipuk G, Galigniana MD (2000). "Oxidative stress induced by L-buthionine-(S,R)-sulfoximine, a selective inhibitor of ...
TY - JOUR. T1 - Effect of L-buthionine-(S,R)-sulphoximine, an inhibitor of γ-glutamylcysteine synthetase on peroxynitrite- and endotoxic shock-induced vascular failure. AU - Cuzzocrea, Salvatore. AU - Zingarelli, Basilia. AU - OConnor, Michael. AU - Salzman, Andrew L.. AU - Szabo, Csaba. PY - 1998. Y1 - 1998. N2 - 1. Peroxynitrite, a cytotoxic oxidant formed from the reaction of nitric oxide (NO) and superoxide is a mediator of cellular injury in ischaemia/reperfusion injury, shock and inflammation. Here we investigated whether L-buthionine-(S,R)-sulphoximine (BSO), an inhibitor of γ-glutamylcysteine synthetase, alters endothelial and vascular smooth muscle injury in response to peroxynitrite in vitro and during endotoxic shock in vivo. 2. In human umbilical vein endothelial cells and in rat aortic smooth muscle cells, BSO (1 mM, for 24 h) enhanced, whereas glutathione (3 mM) or glutathione ethyl ester (3mM) attenuated the peroxynitrite (100-1000 μM)-induced suppression of mitochondrial ...
Depletion of glutathione (GSH) in MCF-7 and MDA-MB-231 cell lines by pretreatment with the GSH synthesis inhibitor buthionine sulfoximine potentiated the activity of 10,11-methylenedioxy-20(S)-camptothecin, SN-38 [7-ethyl-10-hydroxy-20(S)-camptothecin], topotecan, and 7-chloromethyl-10,11-methylenedioxy-20(S)camptothecin (CMMDC). The greatest potentiation was observed with the alkylating camptothecin CMMDC. Buthionine sulfoximine pretreatment also increased the number of camptothecin-induced DNA-protein crosslinks, indicating that GSH affects the mechanism of action of camptothecin.
The results of this study show that, in Sprague-Dawley rats, oxidative stress increased BP, which was associated with renal AT1R upregulation and exaggerated signaling. In BSO-treated rats, Ang II caused significantly higher NKA stimulation and failed to cause inhibition of NKA activity, as seen in control rats. Our data shows that AT1R-mediated NKA stimulation by low Ang II concentration involves MAP kinase, whereas the inhibition at high Ang II concentration involves NO-cGMP signaling. Interestingly, whereas picomolar concentration of Ang II showed robust stimulation of MAP kinase in BSO-treated rats, it failed to activate NO-cGMP signaling and inhibit NKA activity at micromolar concentrations. In control rats, Ang II stimulated NADPH oxidase, but the activation of this enzyme was much higher in BSO-treated rats. In addition, Ang II-mediated, AT1R-dependent O2•− production was also contributed by NOS in BSO-treated rats. Furthermore, Ang II-mediated Pyk2 stimulation was also higher in ...
Cancer stem cells (CSCs) exhibit lower intracellular reactive oxygen species (ROS) levels than non-CSCs, which may be due to the increased expression of free radical scavenging systems. Exogenous agents may be useful to increase ROS and selectively kill CSCs by oxidative stress. Here we tested a combination approach to increase ROS as an effective strategy to eradicate breast CSCs and metastases. Buthionine sulfoximine (BSO) and auranofin (AU) were used to deplete glutathione (GSH) and inhibit thioredoxin reductase (TR), respectively, while mitochondrial-targeted decyltriphenylphosphonium (dTPP) was used to elevate ROS levels. In vitro clonogenicity assays using SUM159 cells showed that treatment with dTPP alone resulted in ,30% survival, while AU+BSO, BSO+dTPP and AU+BSO+dTPP all resulted in ,1% survival. These effects were reversible with N-acetylcysteine pre-treatment. The Aldefluor+ (CSC) population was also measured following drug treatment in vitro. dTPP or AU treatment alone resulted in ...
We investigated the toxicity of hemoglobin/myoglobin on endothelial cells under oxidative stress conditions that include cellular hypoxia and reduced antioxidant capacity. Bovine aorta endothelial cells (BAECs), grown on microcarrier beads, were subjected to cycles of hypoxia and reoxygenation in a small volume of medium, and endothelial cell monolayers were depleted of their intracellular glutathione (GSH) by treatment with buthionine sulfoximine. Incubation of diaspirin cross-linked hemoglobin (DBBF-Hb) or horse skeletal myoglobin (Mb) with BAECs subjected to 3 h of hypoxia caused transient oxidation of the hemoproteins to the ferryl form (Fe(4+)). Formation of the ferryl intermediate was decreased in a concentration-dependent manner by the addition of L-arginine, a substrate of NO synthase, after 3 h of hypoxia. Optimal inhibition of ferryl formation, possibly due to the antioxidant action of NO, was achieved with 900 microM L-arginine. Addition of hydrogen peroxide to GSH-depleted cells in the
A chlorambucil (CLB)-resistant cell line, N50-4, was developed from the established mouse fibroblast cell line NIH 3T3, by multistep drug selection. The mutant cells exhibited greater than 10-fold resistance to CLB. Alterations in GSH and glutathione S-transferase (GST) were found in CLB-resistant variants. A 7-10-fold increase in cellular GSH content and a 3-fold increase in GST activity were detected in N50-4 cells, compared with parental cells, as determined by enzymatic assays. An increase in steady state levels of the GST-alpha isozyme mRNA was found in the CLB-resistant cells, as analyzed by Northern blotting. No GST gene amplification or rearrangement was shown by Southern blot analysis. To test the relative roles of GSH and GST in CLB resistance, a number of GSH- and GST-blocking agents were used. The CLB toxicity was significantly enhanced in N50-4 cells by administration of either the GSH-depleting agent buthionine sulfoximine or the GST inhibitors ethacrynic acid or indomethacin. The ...
Administration of cyclophosphamide at a dose which is lethal to 10% of control athymic nude mice resulted in sudden death within 3 h in all mice that had been pretreated with the glutathione synthesis inhibitor l-buthionine-SR-sulfoximine. In Fischer 344 rats pretreated with l-buthionine-SR-sulfoximine, the cyclophosphamide dose producing 100% acute toxicity was lowered from 500-150 mg/kg; cardiac monitoring revealed ventricular fibrillation to be the cause of death. These and additional studies reported demonstrate that cytoplasmic glutathione is an important protectant against the cardiac and skeletal muscle toxicity of cyclophosphamide and indicate that such toxicity may be substantially increased by glutathione depletion. Since diet and many drugs (including cyclophosphamide itself) are known to affect glutathione levels, the present studies suggest that cardiac and skeletal muscle glutathione content is likely to be a clinically significant determinant of the frequency and severity of the ...
Purpose:Cancer cells (relative to normal cells) demonstrate increased steady-state levels of hydroperoxides that are compensated for by increased glucose and hydroperoxide metabolism. The current study determined if inhibitors of glucose and hydroperoxide metabolism could induce chemo-radio-sensitization by enhancing oxidative stress in lung cancer cells. Experimental Design:A549 and NCI-H292 human lung carcinoma cells were treated with 2-Deoxy-D-glucose (2DG) combined with carboplatin (carbo) + ionizing radiation (IR). Lung cancer cells were further sensitized with inhibitors of glutathione- and thioredoxin-dependent metabolism [buthionine sulfoximine (BSO) and auranofin (Au), respectively] in vitro and in vivo. Results:When 2DG was combined with carbo+IR, clonogenic cell killing was enhanced in A549 and NCI-H292 cells and this combination was more effective than paclitaxel+carbo+IR. The thiol antioxidant (N-acetylcysteine, NAC) was capable of protecting cancer cells from 2DG+carbo-induced cell ...
Have you ever heard of glutathione (pronounced; gloota-thigh-own)? Neither has almost anyone else. Many researchers say its probably the most important substance we require to stay healthy. Many go as far to say its the secret to prevent aging. So wheres Oprah, and the rest of the media? A quick search of the term "glutathione" on PubMed.gov reveals 94,117 scholarly articles, reviews and abstracts. Present in every cell of our body, glutathione levels just might be one of the best biochemical markers there is; the higher your glutathione levels are the healthier you will be. Glutathione deficiency is found in almost all patients with extreme illnesses, e.g., cancer, heart disease, Parkinsons disease, Alzheimers, arthritis, liver disease, diabetes and more. In fact, researchers are concluding glutathione deficiency may play a role in patients with schizophrenia. In cerebrospinal fluid of drug-free schizophrenic patients, a significant decrease in the level of total glutathione was observed ...
Routine cell line maintenance involves removal of waste products and replenishment of nutrients via replacement of cell culture media. Here, we report that routine maintenance of three discrete cell lines (HSB-CCRF-2 and Jurkat T cells, and phaeo-chromocytoma PC12 cells) decreases the principal cellular antioxidant, glutathione, by up to 42% in HSB-CCRF-2 cells between 60 and 120min after media replenishment. However, cellular glutathione levels returned to baseline within 5h after passage. The decrease in glutathione was associated with modulation of the response of Jurkat T cells to apoptotic and mitogenic signals. Methotrexate-induced apoptosis over 16h, measured as accumulation of apoptotic nucleoids, was decreased from 22 to 17% if cells were exposed to cytotoxic agent 30min after passage compared with cells exposed to MTX in the absence of passage. In contrast, interleukin-2 (IL-2) production over 24h in response to the toxin phytohaemagglutinin (PHA), was increased by 34% if cells were challenged
• Critical illness is associated with both immunosuppression and glutathione deficiency. We determined if in vivo depletion of glutathione would adversely affec
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CONICET Digital, el repositorio institucional del CONICET, un servicio gratuito para acceder a la producción científico-tecnológica de investigadores, becarios y demás personal del CONICET.
The effect of photodynamic therapy (PDT) on neurons is of critical importance when treating cancers within or adjacent to the nervous system. Neurons show reduced sensitivity to meta-tetrahydroxyphenyl chlorin (mTHPC) mediated PDT, so the aim of this study was to investigate whether neuron sparing is due to endogenous cellular antioxidant activity. Dorsal root ganglion (DRG) neurons and their associated satellite glia were subjected to mTHPC-PDT in a 3D co-culture system following incubation with antioxidant inhibitors: diethyl dithiocarbamate (DDC, SOD-1 inhibitor), 2-methoxyestradiol (2-MeOH2, SOD-2 inhibitor) and l-buthionine sulfoximine (l-BSO, glutathione synthase inhibitor). Sensitivity of each cell type was assessed using a combination of live/dead staining and immunofluorescence. Pretreatment with DDC and with l-BSO significantly increased the sensitivity of neurons to mTHPC-PDT and also affected satellite glial cell viability, whereas 2-MeOE2 caused only a small increase in neuron ...
TY - JOUR. T1 - Protective effect of glutathione on the cytotoxicity caused by a combination of aluminum and iron in suspension-cultured tobacco cells. AU - Yamaguchi, Yukiko. AU - Yamamoto, Yoko. AU - Ikegawa, Hiroshi. AU - Matsumoto, Hideaki. PY - 1999/3. Y1 - 1999/3. N2 - The role of endogenous glutathione (GSH) in the protection of suspension-cultured tobacco cells from aluminum (Al) toxicity was examined. Cells at the logarithmic phase of growth were treated with or without A1 in nutrient medium prepared without P(i) and EDTA. In the absence of A1, total GSH content (including oxidized glutathione [GSSG]) increased gradually. In the presence of Al, the increase of GSH was repressed. This effect was observed before the loss of plasma membrane integrity and the loss of cell viability. In contrast, GSSG content in cells increased in the presence of A1. GSH-deprived cells were prepared by culturing cells with buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) for 24 h. ...
Background: The role of mesenchymal stem cell in cellular therapy is the subject of interest for many researchers. The differentiation potential of MSCs and abilities in modulations of the recipients immune system makes them important cells in tissue regenerative studies. MSCs by releasing the proinflammatory cytokines play important role in immunomodulatory systems; however the signaling pathways for releasing of these mediators are not well understood. Glutathione has been shown to play a role in modulation of cytokines in hepatogenic differentiation. Objective: In the current study we aimed to investigate the effects of buthionine sulfoximine (BSO, inhibitor for glutathione synthesis) and N-acetylecystin (NAC, an inhibitor for ROS generation) on proinflammatory cytokines production in a hepatogenic differentiation model. Results: BSO and NAC significantly decreased IL-6 and TNF-α levels at 14 days of differentiation, whereas, NAC decreased the levels of IL-8 at days 2 and 14 of differentiation.
Arsenic trioxide (As2O3) has shown anti-tumour activity against a variety of solid tumours in vitro. However, the mechanisms responsible for its cytotoxicity against ovarian carcinoma remain elusive. In this thesis, the molecular determinants of its effects and factors mediating its chemoresistance in ovarian cancer cells were investigated. It was found that As2O3 treatment caused both apoptosis induction and caspase-independent cell death involving mitochondrial dysfunction. This was accompanied by endoplasmic reticulum stress induction and an increase in intracellular glutathione (GSH) level. The latter was in turn prevented by the concurrent use of GSH modulator, buthionine sulfoximine but not ascorbic acid. Gene expression analysis of arsenic-resistant OVCAR-3 (OVCAR-3/AsR) cells showed the involvement of multiple factors mediating its chemoresistance. Of particular interest, a genetic hub involving elevated interleukin 1A signalling was identified. This could consecutively modulate the ...
Villablanca JG, Volchenboum SL, Cho H, Kang MH, Cohn SL, Anderson CP, Marachelian A, Groshen S, Tsao-Wei D, Matthay KK, Maris JM, Hasenauer CE, Czarnecki S, Lai H, Goodarzian F, Shimada H, Reynolds CP. A Phase I New Approaches to Neuroblastoma Therapy Study of Buthionine Sulfoximine and Melphalan With Autologous Stem Cells for Recurrent/Refractory High-Risk Neuroblastoma. Pediatr Blood Cancer. 2016 08; 63(8):1349-56 ...
In this study, we developed an in vivo method to determine drug effects on oxidation-induced apoptosis in the zebrafish brain caused by treatment with l-hydroxyglutaric acid (LGA). We confirmed that LGA-induced apoptosis was caused by oxidation by examining the presence of an oxidative product, nitrotyrosine. Next, we examined the effects of 14 characterized neuroprotectants on LGA-treated zebrafish, including: d-methione (d-Met), Indole-3-carbinol, deferoxamine (DFO), dihydroxybenzoate (DHB), deprenyl, l-NAME (N(G)-nitro-l-arginine methyl ester), n-acetyl l-cysteine (l-NAC), 2-oxothiazolidine-4-carboxylate (OTC), lipoic acid, minocycline, isatin, cortisone, ascorbic acid and α-tocopherol. Eleven of 14 neuroprotectants and 7 of 7 synthetic anti-oxidants exhibit significant protection in zebrafish. Buthionine sulfoximine (BSO), used as a negative control, exhibited no significant protective effects. In addition, three blood-brain barrier (BBB) impermeable compounds exhibited no significant effects. Our
Chemicals. [3H]Vincristine (2.5 Ci/mmol), [3H]digoxin (55 mCi/mmol), and ritonavir were purchased from Moravek Biochemicals (Brea, CA). Anti-actin (clone AC-40), l-buthionine-[S,R]-sulfoximine (BSO), digoxin, EDTA, indomethacin, genistein, probenecid, and sulfinpyrazone were purchased from Sigma-Aldrich (Oakville, ON, Canada). MK571 and indinavir were a kind gift from Merck Research Labs (West Point, PA). Saquinavir was kindly provided from Roche Diagnostics (Hertfordshire, UK). The monoclonal antibodies MRPr1 and M2III-6 were purchased from Kamiya Biomedical (Seattle, WA).. Cell Culture. The microglia cell line (MLS-9) was derived from neopallia of 2- or 3-day-old Wistar rat pups, as described previously (Zhou et al., 1998; Cayabyab and Schlichter, 2002). Briefly, microglia were isolated by enzymatic dissociation of tissue, and cultured in endotoxin-free medium (Invitrogen, Burlington, ON, Canada) for 10 to 12 days without feeding. Essentially pure microglia cultures (,98% as determined by ...
Glutathione deficiency can still be treated and restored to satisfactory levels once again. Knowing how to increase the glutathione in your body is the first step.
Egea, J., Fabregat, I., Frapart, Y. M., Ghezzi, P., Görlach, A., Kietzmann, T., Kubaichuk, K., Knaus, U. G., Lopez, M. G., Olaso-Gonzalez, G., Petry, A., Schulz, R., Vina, J., Winyard, P., Abbas, K., Ademowo, S., Afonso, C. B., Andreadou, I., Antelmann, H., Antunes, F., Aslan, M., Bachschmid, M. M., Barbosa, R. M., Belousov, V., Berndt, C., Bernlohr, D., Bertrán, E., Bindoli, A., Bottari, S. P., Brito, P. M., Carrara, G., Casas, A. I., Chatzi, A., Chondrogianni, N., Conrad, M., Cooke, M. S., Costa, J. G., Cuadrado, A., My-Chan Dang, P., De Smet, B., Debelec-butuner, B., Dias, I., Dunn, J. D., Edson, A. J., El Assar, M., El-Benna, J., Ferdinandy, P., Fernandes, A. S., Fladmark, K. E., Förstermann, U., Giniatullin, R., Giricz, Z., Görbe, A., Griffiths, H., Hampl, V., Hanf, A., Herget, J., Hernansanz-Agustín, P., Hillion, M., Huang, J., Ilikay, S., Jansen-Dürr, P., Jaquet, V., Joles, J. A., Kalyanaraman, B., Kaminskyy, D., Karbaschi, M., Kleanthous, M., Klotz, L-O., Korac, B., Korkmaz, K. S., ...
Glutathione plays a pivotal role in many key metabolic reactions in your body. Each of your cells contains glutathione, a substance created from three amino acids: cysteine, glutamate, and glycine. The bodys
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Highlights aus dem Helmholtz-Zentrum Dresden-Rossendorf (HZDR) 2010, Inhalt, Ueberblick, Investitionen in die Zukunft - Grusswort des Vorstands, Ereignischronik 2010, Highlights aus der Forschung, Zukunftsprojekte, Nachwuchs, Wissens- und Technologietransfer, Preise - Rufe - Personalia, Impressum
FINALLY! Tonight at 8:00 PM eastern time, the most anticipated season in NBA history kicks off as the Boston Celtics host the Miami Heat and their new Big Three
Das GDNF-Gen kodiert einen von Glia-Zellen gebildeten neutrotrophischen Faktor der zusammen mit dem Produkt des RET-Gens die Bildung und Apoptose von Nervenzellen steuert. Mutationen führen zu verschiedenen autosomal dominanten Erkrankungen, dem zentralen Hypoventilationssyndrom, der Hirschsprung-Erkrankung und dem Phäochromozytom.. ...
Die Jungs vom GLOBUS Supermarkt sind echte Garanten für lustige Schreibfehler. Das heutige Fundstück stammt aus dem Globus in Koblenz, in dem Grichische
Die Diagnostik und Behandlung von akuten Angio demen ist anspruchsvoll. Es handelt sich um klinisch leicht verwechselbare Krankheitsbilder, die aufgrund unterschiedlicher pathophysiologischer Mechanismen entstehen. Zu den ausl senden Faktoren z hlen...
Die Jungs vom GLOBUS Supermarkt sind echte Garanten für lustige Schreibfehler. Das heutige Fundstück stammt aus dem Globus in Koblenz, in dem Grichische
Wenn du auf dem Klo sitzt und nicht weisst, was du ohne dein Handy mit dem Leben...3. Wenn dein Handy einen Ehrenplatz in deinem Bett hat ...
Unter wel-chen Vor-aus-set-zun-gen ist die Kün-di-gung eines Wohn-raum-miet-ver-hält-nis-ses wegen beab-sich-tig-ter wirt-schaft-li-cher Ver-wer-tung des Grund-stücks nach § 573 Abs. 2 Nr. 3 BGB (hier: zur Erwei-te-rung eines benach-bar-ten Mode-hau-ses) wirk-sam? Mit die-ser Fra-ge hat-te sich aktu-ell der Bun-des-ge-richts-hof zu befas-sen: Anlass hier-für bot ihm ein Fall aus dem Schwarz-wald: Die Mie-ter haben im. Lesen ...
Dobrý večer, viete mi poradiť tinktúry na môj problém? V januári, som bola na kyretaž polypov v maternici, následné v marci som...
Henoch-Schönlein purpura (HSP) is typically seen as a self-limiting disease in children, but can present more severely in adults, especially when there is renal involvement. Management of HSP in adults also remains a controversial topic with very few studies evaluating available therapies. In this case, HSP presenting as a combination of severe gastrointestinal involvement and a rapid decline in renal function in an adult patient directed our therapy. The patient was a 48-year-old Caucasian male with no known past medical history, who presented with a combination of purpuric rash over the lower extremities, severe abdominal pain with upper gastrointestinal bleeding and a rapidly increasing serum creatinine, with hematuria ...
Define L-phenylalanine mustard. L-phenylalanine mustard synonyms, L-phenylalanine mustard pronunciation, L-phenylalanine mustard translation, English dictionary definition of L-phenylalanine mustard. n a drug, C13H18Cl2N2O2, used to treat myeloid leukaemia Noun 1. melphalan - antineoplastic drug used to treat multiple myeloma and some other malignancies...
This study examined the effect of glutathione on the in vivo depigmenting potency of N-acetyl-4-S-cysteaminylphenol (N-acetyl-4-S-CAP) in black and yellow mice after multiple intraperitoneal injections on 10 consecutive days. In black mice (C57BL/6J, a/a), N-acetyl-4-S-CAP showed dose-dependent depigmenting potency (0.5, 1.0, and 2.0 mmol/kg), which was in parallel to the tissue eumelanin content (98%, 28%, and 3% of controls, respectively) and to the tissue glutathione content (94%, 85%, and 76%, respectively). In lethal yellow mice (C57BL/6J, Ay/a), only a dose of 2.0 mmol/kg showed the color change of hair to dark, not to white as seen in black mice. This was reflected by the decrease of pheomelanin content (56%) and the increase of eumelanin content (28% of black mice). The simultaneous administration of N-acetyl-cysteine, which up-regulated glutathione content, completely abolished the depigmenting potency of N-acetyl-4-S-CAP, whereas administration of buthionine sulfoximine, which depleted ...
PURPOSE: To characterize glutathione (GSH) transport by cultured human retinal pigment epithelial (HRPE) cells. METHODS: Cultured HRPE cells were pretreated with acivicin for GSH efflux and with buthionine sulfoximine for GSH uptake to prevent the breakdown and resynthesis of GSH. Efflux was measured by the linear rate of accumulation of GSH in the supernatant; uptake was measured using [35S] GSH plus varying concentrations of GSH. Molecular forms were verified by high-performance liquid chromatography. HRPE cell mRNA was probed for the presence of the two recently cloned rat sinusoidal and canalicular GSH transporters, (RsGshT and RcGshT), by Northern blot analysis. RESULTS: Glutathione efflux was temperature dependent (undetectable at 4 degrees C), and its averaged 23 +/- 3.3 pmol/10(6) cells/minute or 10% of the total GSH effluxed per hour (total cell GSH = 13.6 +/- 1.5 nmol/10(6) cells). Efflux was not influenced by dithiothreitol or sulfobromophthalein-reduced GSH adduct, agents known to ...
Correction of glutathione deficiency in the lower respirat-ory tract of HIV seropositive individuals by glutathione aerosol treatment Academic Article ...
Three synthetic methodologies are studied in details in this dissertation. For 1,5-hydride shift of alkenyl sulfoximine methodology, the reaction mechanism was studied using deuterium labeling. An uncommon 6-endo-trig 1,5-hydride shift process was discovered. The scope and limitation were studied using N-alkyl, N-allyl, and N-benzyl-substituted S-alkenyl sulfoximines. N-H-S-alkyl sulfoximines, four- and six-membered heterocyclic rings and a new class of chiral dienes were obtained. In [4+3] cycloaddition and ring opening chapter, we demonstrated an ene-like reaction using a symmetric oxyallylic cation can provide α-substituted cyclopentenones. Enantio pure products are potentially accessible by this method. [4+3] Cycloaddition of the symmetric oxyallylic cation with substituted furans, and the ring-opening process of the resulting 8-oxabicyclo[3.2.1]oct-6-en-3-one were also studied. The reaction conditions and scope were investigated. An acid-catalyzed mechanism was proposed for the ...
Effect of BSO on the Toxicity of the Camptothecins. To assess the contribution of GSH in the sensitivity to the camptothecins, cells were pretreated with BSO before the cytotoxicity assays. BSO is an inhibitor of γ-glutamylcysteine synthetase, the rate-limiting enzyme in GSH biosynthesis (23). Treatment of MCF-7 and MDA-MB-231 cells for 24 h with 50 μm BSO led to a reduction in GSH levels of at least 75% in the cell lines tested (Table 1) without affecting cell growth. Pretreatment with BSO also resulted in lower IC50 values for each of the analogues tested in all of the cell lines (Table 1). GSH depletion had the greatest effect on CMMDC, the alkylating camptothecin analogue.. Effect of BSO on the Formation of topo I-DNA Complexes. To determine whether GSH depletion directly affected the stabilization of the camptothecin-topo I cleavage complex, the levels of camptothecin-induced DPCs were measured in control cells and in cells pretreated with BSO. These DPCs correspond to topo I cleavage ...
N,N-Diethylethanamine;ethyl dihydrogen phosphate | C14H37N2O4P | CID 111941 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
Glutathione biosynthesis and transporter genes are only induced after Zn + Cd treatment in leaves of the metallicolous genotype and thus display category (3)
HIV infection is associated the development of increased oxidative stress and deficiency of glutathione (GSH), the dominant endogenous antioxidant protein, but the underlying mechanisms contributing to GSH deficiency are hitherto unknown. Furthermore GSH metabolism has not been studied in HIV patients, in whom the burden of risk factors promoting oxidative stress is highest. Our previous studies in non-HIV human subjects with diabetes-related oxidative stress and GSH deficiency have demonstrated that the latter is due to decreased synthesis of GSH. Importantly, short-term dietary supplementation with the simple GSH precursor amino-acids cysteine and glycine, boosted GSH synthesis and cellular concentrations, corrected GSH deficiency, and reduced oxidative stress and oxidant damage. The current proposal will study whether (1) defective synthesis underlies GSH deficiency in patients with HIV, and will test a simple, inexpensive and rational therapy based on protein supplementation to improve GSH ...
In our article on arthritis, we talked about a mix of nutrients that can dramatically decrease arthritis pain over six weeks. One of these is a simple and cheap nutrient called MSM. This sulfur-containing compound helps supply the sulfur needed for the proteins that heal tissues. Another recent study showed that MSM also suppresses inflammation and the inflammatory molecules (cytokines) that cause inflammation. Now a new study shows that MSM also increases the critical antioxidant glutathione. Many people theorize that glutathione deficiency is one of the key common underlying problems that causes Chronic Fatigue Syndrome.
Oxidative stress happens once theres associate degree imbalance between the assembly of free radicals and also the bodys ability to fight them off. Too-high levels of aerobic stress is also a precursor to multiple diseases. These embrace polygenic disease, cancer, and atrophic arthritis. Glutathione helps avert the impact of aerobic stress, which may, in turn, cut back illness.. An article cited in Journal of Cancer Science and Therapy care indicated that glutathione deficiency results in magnified levels of aerobic stress, which could result in cancer. It conjointly expressed that elevated glutathione levels raised inhibitor levels and resistance to aerobic stress in cancer cells.. Glutathione is a very strong antioxidant, partly because of high concentrations that can be found in every cell in the body. Supplements like George Bridgehams GRS Ultra helps you maintain the optimum level of glutathione and prevent yourself from suffering from various chronic diseases. Moreover, the supplement ...
Nowadays, Fenton reaction-based chemodynamic therapy (CDT) strategies have drawn extensive attention as tumor-specific nanomedicine-based therapy. Nevertheless, current existing CDTs normally suffer from therapeutic bottlenecks such as the scavenging of hydroxyl radical (˙OH) by intracellular antioxidants an
1. Abdel Malik P, Husted J, Chow EW, Bassett AS. Childhood head injury and expression of schizophrenia in multiply affected families. Arch Gen Psychiatry. 2003. 60: 231-6. 2. Aoyama K, Watabe M, Nakaki T. Regulation of neuronal glutathione synthesis. J Pharmacol Sci. 2008. 108: 227-38. 3. Aoyama K, Suh SW, Hamby AM, Liu J, Chan WY, Chen Y. Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. Nat Neurosci. 2006. 9: 119-26. 4. Arand M, Melzner H, Kinzl L, Bruckner UB, Gebhard F. Early inflammatory mediator response following isolated traumatic brain injury and other major trauma in humans. Langenbecks Arch Surg. 2001. 386: 241-8. 5. Aranow C. Vitamin D and the immune system. J Investig Med. 2011. 59: 881-6. 6. Armitage R. Sleep and circadian rhythms in mood disorders. Acta Psychiatr Scand Suppl. 2007. 433: 104-15. 7. Arora K, Alfulaij N, Higa JK, Panee J, Nichols RA. Impact of sustained exposure to β-amyloid on calcium homeostasis and neuronal ...
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Homocysteine is usually broken down into the amino acid cysteine. Cysteine is one of the amino acids needed by the cells to make intracellular glutathione. If your body does not convert homocysteine to cysteine the intracellular glutathione conversion will not take place. ...
Eventbrite - University College of Osteopathy presents BSO Open Day - Wednesday, 13 July 2016 at The British School of Osteopathy (teaching centre), London, Gt Lon. Find event and ticket information.
Boobs: No, not like that. See, we see you feed the baby, and we know that the milk youre giving him isnt from us. Because, you know, were dry. This is the fault line for our shattering identity earthquake. We mean, logically we know that youre giving him artificial milk because youre taking a couple of medications that you really cant go without right now, but we feel cheated. We dried up suddenly and traumatically, and were quite upset about it. ...
Gandl, J., 1987: Die Karbon-Trilobiten des Kantabrischen Gebirges NW-Spanien 4 Trilobiten aus dem hoheren Namur und tieferen Westfal Die Karbon-Trilobiten des Kantabrischen Gebirges NW-Spanien 4 Trilobiten aus dem hoheren Namur und tieferen Westfal
Mastektomia z powodu raka piersi ma na celu doszczętne wycięcie miąższu gruczołu. Konieczność resekcji klinicznie zdrowej tkanki w obrębie fałdu podpiersiowego (ang. inframammary fold - IMF) jest poddawana dyskusji. Usunięcie miąższu także w okolicy IMF może potencjalnie zmniejszyć ryzyko powstania wznowy raka piersi. Jednakże u pacjentek poddawanych operacji odtwórczej zachowanie fałdu podpiersiowego może przyczynić się do uzyskania naturalnie wyglądającej, nieznacznie opadającej, piersi. Odrębnym problemem jest obecność pierwotnego ogniska raka gruczołu piersiowego w okolicy fałdu podpiersiowego. Celem pracy było przedstawienie opisu przypadku pacjentki leczonej z powodu inwazyjnego raka piersi w obrębie IMF oraz analiza onkologicznego aspektu postępowania chirurgicznego z fałdem podpiersiowym podczas mastektomii w odniesieniu do znaczenia tej struktury anatomicznej w rekonstrukcji piersi. Zaprezentowano przypadek 52-letniej kobiety leczonej z powodu guza lewej piersi.
Das Game wurde in einer Kooperation des Instituts für Medien und Schule der Pädagogischen Hochschule Schwyz (vormalig: PHZ Schwyz) und der Studienrichtung Game Design der Zürcher Hochschule der Künste konzeptioniert und entwickelt und ist seit Mai 2011 online frei verfügbar. Mittlerweile gibt es sechs Spielelevel, vier davon beschäftigen sich mit der Beurteilung von Glaubwürdigkeit von Internetinformationen, zwei mit dem Vermeiden von Viren- und Phishingmails. Ein Nationalfondsprojekt zur wissenschaftlichen Überprüfung der Wirksamkeit wurde, bewilligt und durchgeführt (13DPD3_134705). Es endete im März 2014 und zeigte u.a., dass die Beschäftigung mit dem Spiel insgesamt zu besserer Informationskompetenz führt, dass jedoch nicht alle Kinder gleich gut damit lernen. Insbesondere Schülerinnen und Schüler, die in ihrer Freizeit häufig Videogames spielen, zeigen stärkere Lerngewinne mit dem Computerspiel als wenn sie sich auf andere Art und Weise mit dem Thema beschäftigen. ...
Surgery is one of the treatment options offered for individuals with endometriosis. With that in mind, there are a variety of surgical procedures that can be offered…
Kit Component:- KN302221G1, Bola1 gRNA vector 1 in pCas-Guide vector- KN302221G2, Bola1 gRNA vector 2 in pCas-Guide vector- KN302221D, donor vector…
Kunstkreis Atelier im Revierpark Vonderort Oberhausen - offen für alle Künstler aus dem Ruhrgebiet. Der Kunstkreis Atelier im Revierpark Vonderort in Oberhausen ist ein Gemeinschaftsprojekt von vielen Künstlerinnen und Künstlern aus dem Ruhrgebiet. Die Künstlerinnen und Künstler des Kunstkreises Atelier sind durch zahlreiche Kunstausstellungen weit über die Grenzen des Ruhrgebiets hinaus bekannt.
De conformidad con el Decreto 677 de abril 26 de 1995, y demás De conformidad con el Decreto 677 de abril 26 de 1995, y demás normas legales vigentes, la información contenida en este portal está dirigida única y ... ...
Wissenschaftliche Publikationen aus dem Fachbereich Plastische Chirurgie und Gesichtschirurgie des Kölner Arztes Dr. Dr. med. Matthias Siessegger.
Kyoll vermischt mittelalterliche und klassische Instrumente mit elektronischen Beats zu dem ureigenen Endzeitfolk. Stilbrueche sind an der Tagesordnung. Burleske Elemente treffen auf eine Marlene Dietrich der Apokalypse. Barockes Sinnentreiben und kammermusikalische Geigen- und Drehleiersoli komplettieren ein vertörendes Ensemble, das auch einem Mad Max Szenario entsprungen sein könnte.. ...
Ersetzen Sie oben genannten Werte in Ihrem Axon Max mit Werten in jeder Einstellung unten Vodafone alternative Einstellungen, die mit dem Gerät kompatibel sein könnte ...
Operationsziel Ziel ist der Wechsel einer oder beider gelockerten Prothesenkomponenten, um die mit dem periprothetischen Lockerungsprozess verbundenen Schmerzen zu lindern bzw. zu beseitigen und die...
Die Zeitschrift Klinische Pädiatrie veröffentlicht Beiträge aus dem Gebiet der (klinischen) Pädiatrie und deren Grenzgebiete in deutscher und englischer Sprache.
Die Infektion mit dem humanen Immundefizienzvirus (HIV) stellt weltweit eine der bedeutendsten medizinischen Herausforderungen dar. Mit den in westlichen Industrieländern verfügbaren antiretroviralen
Dr. Waleska Haibach-Vega ist seit dem Jahr 2001 im Bereich Refraktive Chirurgie tätig. Sie berät Patienten in unseren EuroEyes AugenLaserZentren München und Augsburg.
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TY - JOUR. T1 - Phenytoin liver glutathione depletion. A possible mechanism of liver injury. AU - Snodgrass, W. R.. AU - Whitfield, S.. PY - 1981. Y1 - 1981. N2 - Phenytoin produces significant liver glutathione depletion in vivo in mice. Pretreatment with inducers and inhibitors of drug metabolism show enhancement of phenytoin-induced glutathione depletion following phenobarbital and 3-methylcholanthrene pretreatment, inhibition of glutathione depletion following piperonyl butoxide, cobaltous chloride and alpha-naphthylisothiocyanate pretreatment (all drug metabolism inhibitors), and prevention of glutathione depletion following butylated hydroxytoluene pretreatment (both inducers of epoxide hydrolase). These data suggest that phenytoin-induced liver glutathione depletion may occur via a reactive metabolite and that this reactive metabolite possibly may be an epoxide.. AB - Phenytoin produces significant liver glutathione depletion in vivo in mice. Pretreatment with inducers and inhibitors of ...
Recent studies have demonstrated that perturbations of intracellular thiol and calcium homeostasis may be important events in the early development of cell injury by toxic chemicals. Incubation of isolated rat hepatocytes in a calcium free medium, severely depleted intracellular Ca²⁺ levels and resulted in the loss of both cytosolic and mitochondrial glutathione (GSH), which preceded cell injury. Elevation of endogeneous a-tocopherol levels, by supplementing the hepatocyte suspension with vitamin E-succinate, inhibited the loss of GSH and reversed cell injury. Increased levels of GSH in the presence of vitamin E-succinate were induced by an apparent a-tocopherol-mediated effect on GSH biosynthesis, indicating a close relationship between these two important cellular antioxidant systems. Perturbation of intracellular calcium homeostasis in hepatocytes by the administration of A23187, a calcium ionophore, in the presence of different concentrations of extracellular Ca²⁺ , revealed a striking ...
Glutamate-cysteine ligase, also known as gamma-glutamylcysteine synthetase is the first rate-limiting enzyme of glutathione synthesis. The enzyme consists of two subunits, a heavy catalytic subunit and a light regulatory subunit. This locus encodes the catalytic subunit, while the regulatory subunit is derived from a different gene located on chromosome 1p22-p21. Mutations at this locus have been associated with hemolytic anemia due to deficiency of gamma-glutamylcysteine synthetase and susceptibility to myocardial infarction.[provided by RefSeq, Oct 2010 ...
A: Glutathione deficiency is a serious medical problem, and is associated with anemia, loss of coordination, and muscle stiffness, among other symptoms. Deficiency in glutathione is usually caused by a genetic mutation, so in these cases, supplementation is typically not helpful. Lower, but still biologically normal, levels of glutathione dont have a well-characterized symptom set. Glutathione supplementation, as discussed earlier, might be helpful for improving antioxidant status and immune function, though. Q: What does glutathione do to your skin? A: Glutathione has achieved rapid popularity as a way to lighten skin, with the thought that melanin in skin will undergo structural changes in response to the increased antioxidant activity of glutathione. Unfortunately, according to a review of the latest medical research published in the journal Dermatology Practical & Conceptual, there are no high-quality studies suggesting that glutathione can actually lighten skin to a significant degree (7). ...
OUTLINE: This is a dose-escalation, two-stage, multicenter study.. During stage I, patients receive a single dose of dimesna IV over 15 minutes 7 days prior to chemotherapy. Patients then receive paclitaxel IV over 3 hours followed by dimesna IV over 15-30 minutes followed immediately by cisplatin IV over 1 hour on day 1 every 3 weeks. Patients continue courses of paclitaxel, dimesna, and cisplatin every 3 weeks in the absence of disease progression or unacceptable toxicity for up to 6 courses.. In stage I, cohorts of 3-6 patients each receive escalating doses of dimesna until the maximum tolerated dose (MTD) is reached. The MTD is defined as the highest dose at which no more than 1 of 6 patients experiences dose limiting toxicity (DLT). The MTD of dimesna is then used in stage II of the study, in which the volume of pre and post cisplatin intravenous saline hydration is reduced in cohorts of 3-6 patients each. The MTD intensity of cisplatin is defined as the least saline hydration volume at ...
Bei manchen Anwendungen der im Patent 191 von Brockway et al. In some applications in patent 191 Brockway et al. beschriebenen Druckme vorrichtung kann das Geh use aufgrund physikalischer Einschr nkungen und praktischer berlegungen hinsichtlich des chirurgischen Prozesses nicht in unmittelbarer N he des Bereiches implantiert werden, in dem der Druck zu messen ist. The pressure measurement device described, the housing can due to physical limitations and practical considerations of the surgical process not be implanted in the immediate vicinity of the area in which the pressure is to be measured. Wenn sich das Geh use nicht in unmittelbarer N he des Bereiches befindet, in dem der Druck zu messen ist, kann die dann erforderlich werdende L nge des Katheters zu gro werden, so da Fehler, die sich aus dem dann schlechteren dynamischen Verhalten oder bei einer nderung der Haltung ergeben, f r die jeweilige Anwendung nicht mehr innerhalb akzeptabler Grenzen liegen. If not, the housing is located in ...
Glutathione (GSH) Is A Critical Mineral and An Important Intracellular Antioxidant GSH regulates all other antioxidants, while preventing damage to importan...
Previously we found that a decrease in glutathione (GSH) concentration is a general phenomenon in aging organisms. This suggested our hypothesis that the capacity for detoxification involving GSH will decrease in senescence. Thus the present objectives were to determine the toxicity of acetaminophen (APAP) and its relationship to GSH status in the aging mosquito. Different concentrations of APAP in Aedes Ringer were injected into adult mosquitoes of different ages through the life-span. The results showed that the LD50 values were highest in the young adult, plateaued in the mature, and decreased 7-fold in the very old adults (p less than 0.0001). Of special interest was that these decreasing LD50 values were closely correlated with the aging-specific decreases in GSH concentration observed in our previous experiments (r = 0.99). Also a direct relationship was established as the administration of a lethal dose (LD50) of APAP depleted more than 99% of the GSH content (p less than 0.0001). This is ...
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Der diesjährige Schwerpunkt des Kongresses liegt auf den Themen Trauma und Tumor in der Wirbelsäulenchirurgie. Wichtige wissenschaftliche Beiträge zu Tumorerkrankungen, degenerativen Erkrankungen, entzündlichen und metabolischen Erkrankungen, Verletzungen und Deformitäten aber auch zu innovativen Techniken erwarten die Besucherinnen und Besucher. Dabei steht ein fächerübergreifender Ansatz im Vordergrund, denn auch auf dem Gebiet der Wirbelsäulenheilkunde gilt es, Bewährtes zu erhalten und gleichzeitig neuen Behandlungsmethoden gegenüber offen zu sein. Dass die Deutsche Wirbelsäulengesellschaft diesen Anspruch ernst nimmt, zeigt auch die Zentren-Zertifizierung, die in diesem Jahr gestartet wurde. (Mehr in: Veranstaltungen - idw - Informationsdienst Wissenschaft). - Weiterlesen ...
Ein einfaches Verfahren zur Züchtung der Tuberkelbazillen aus dem Sputum. Acta Litterarum ac Scientiarum Regiae Universitatis Hungaricae Francisco-Josephinae : sectio medicorum, (4). pp. 87-90. (1929 ...
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Liebe Leserinnen und Leser, in Hamburg hat sich nach dem Tod der 11jährigen Chantal, die im Januar an einer Methadonvergiftung starb, ein Runder Tisch gebildet, an dem VertreterInnen der zuständigen Behörden und Jugendämter, der Kassenärztlichen Vereinigung, der Ärztekammer und der substituierenden Ärzte überlegen, wie zukünftig mit SubstitutionspatienInnen umgegangen werden soll, in deren Haushalt minderjährige Kinder leben. Sollen diese PatientInnen prinzipiell eine Schweigepflichtentbindung gegenüber dem Jugendamt unterzeichnen? Soll grundsätzlich oder anlassbezogen gemeldet werden? Reicht das Kinderschutzgesetz aus, im Verdachtsfall die Aufmerksamkeit der Jugendämter auf diese Familien zu lenken? Welche Verbesserungen benötigen die Substitutionsbehandlung und deren Qualitätskontrolle durch die KV? Ziel ist ein Kooperationsvertrag zwischen Behörden und Ärzteschaft, der bis zum Sommer ausgearbeitet werden soll. Die Chronik der Ereignisse: Anhang: dgs-info_60_Der Tod von ...
Weider Beta-Alanine 120 Kapsel (154g) Dose Dosierung und t gliche Verzehrempfehlung: 2 Kapseln nach dem Fr hst ck und 2 Kapseln vor dem Training An training
Der Konsum von Kokain führt zu einer Überaktivität des Nervensystems. Das wiederum kann nicht nur zu einem Mangel an Neurotransmittern führen, sondern kann dem ganzen Körper schaden. Ein Mangel an Neurotransmittern führt zu Schlaflosigkeit, vermindertem Antrieb, Depressionen und einem allgemeinen Gefühl eines schweren Katers.. After C enthält die richtige Zusammenstellung von Nahrungsergänzungsmitteln und Vitaminen, um zu helfen, daß die negativen Effekte auf einem Minimum gehalten werden. Am Morgen nach dem Sündigen, je eine dieser 3 Kapseln mit ausreichend Wasser schlucken.. ...
Post contrast axial CT. Post contrast axial CT scan demonstrating a heterogeneous, well circumscribed lesion in the left pre-epiglottic space abutting the poste
Die Flash-Chromatographie ist die bevorzugte Reinigungsmethode für organische Stoffe, Arzneimittel und Naturstoffe. In jüngster Zeit hat sie auch die Peptidchemie erobert, verfügt sie doch über die Fähigkeit, eine Vielzahl unterschiedlicher Verbindungen effizienter zu trennen, als dies mit anderen Vorreinigungsverfahren wie z. B. dem Ausfällen (Protein-Crash) oder der Flüssig-Flüssig-Extraktion möglich ist. Zur Herstellung reiner Verbindungen können Chemiker je nach dem gewünschten Reinheitsgrad auf eine Vielzahl unterschiedlicher Variablen zurückgreifen. In diesem Whitepaper möchten wir die Faktoren erläutern, die für eine erfolgreiche Aufreinigung mithilfe der Flash-Chromatographie kontrolliert werden müssen ...
Spuren der römischen Ärzte auf dem Boden der Schweiz, von Dr. med. Conrad Brunner,... Nach einem am 26. Januar 1893 im Rathaus in Zürich gehaltenen akademischen Vortrage ...
Recherchieren Sie hier nach Experten und Ansprechpartnern zur Forschung. Alle Daten werden aus dem Forschungsportal Sachsen-Anhalt http:// www.forschung-sachsen-anhalt.de und dem LSF der Otto-von-Guericke-Universität Magdeburg (OVGU) entnommen.
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55th Civil Court Dist Rep Dem None Rep% Dem% Under% ====================================================== HD126 30,233 24,644 1,355 55.09% 44.91% 10.85% HD127 42,637 24,900 1,574 63.13% 36.87% 10.12% HD128 35,499 16,006 1,166 68.92% 31.08% 10.70% HD129 37,342 26,324 2,023 58.65% 41.35% 12.24% HD130 52,602 22,821 1,669 69.74% 30.26% 10.04% HD131 6,328 35,416 803 15.16% 84.84% 9.40% HD132 33,591 32,514 1,267 50.81% 49.19% 9.54% HD133 43,482 26,449 2,625 62.18% 37.82% 12.38% HD134 43,229 43,298 4,447 49.96% 50.04% 13.50% HD135 27,503 27,919 1,288 49.62% 50.38% 10.82% HD137 7,664 16,339 651 31.93% 68.07% 12.07% HD138 24,343 23,390 1,477 51.00% 49.00% 12.93% HD139 11,101 35,586 1,187 23.78% 76.22% 11.00% HD140 5,470 17,978 604 23.33% 76.67% 14.49% HD141 4,035 27,344 456 12.86% 87.14% 8.83% HD142 8,754 30,706 762 22.18% 77.82% 9.07% HD143 7,706 20,648 883 27.18% 72.82% 14.69% HD144 9,282 13,946 589 39.96% 60.04% 13.11% HD145 10,224 22,188 1,053 31.54% 68.46% 13.19% HD146 8,664 34,224 1,237 20.20% ...
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Recherchieren Sie hier nach Experten und Ansprechpartnern zur Forschung. Alle Daten werden aus dem Forschungsportal Sachsen-Anhalt http:// www.forschung-sachsen-anhalt.de und dem LSF der Otto-von-Guericke-Universität Magdeburg (OVGU) entnommen.
Opened 1965 - Closed 1991 Visited with a camera crew for Midlands Today, and the former Commandant of No 16 Group (Shrewsbury). Internally the post...
Kuba är ett samhälle, där det väl finns ett visst mått av Storebror-komplex eller Castro-ser-dig-fasoner. Nu talas det om generation Y på Kuba, och till dem hör 33-åriga Yoani Sánchez, Bloggaren som retar Kuba (DN, 10.1.2009 ...
Das KLB kodiert eine cDNA welches sehr ähnlich dem Klotho ist. Deshalb kann eine ähnliche Funktion oder Interaktion vermutet werden.. ...
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Glutathione metabolism was studied in cancer cells during the growth of an Ehrlich ascites tumour. GSH, but not GSSG, content decreases when cell proliferation and the rate of protein synthesis in the tumour decrease. This change correlates with a decrease in the rate of GSH synthesis and an increase in glutathione peroxidase and glutathione S-transferase activities. Glutathione efflux from tumour cells seems to co-ordinate with the rate of GSH synthesis. Cysteine, and not methionine, promotes GSH synthesis in tumour cells. However, changes in the rate of GSH synthesis are not due to limitations in the supply of blood cysteine or to changes in the intracellular amino acid pool of the cancer cells. Our data suggest that changes in protein metabolism accompanying tumour growth in vivo can modulate glutathione content in cancer cells. ...
TY - JOUR. T1 - Glutathione depletion following inhalation anesthesia. AU - Zumbiel, M. A.. AU - Fiserova-Bergerova, V.. AU - Malinin, Theodore. AU - Holaday, D. A.. PY - 1978/12/1. Y1 - 1978/12/1. N2 - Glutathione depletion following inhalation of halogenated anesthetics was investigated as a possible mechanism of toxic reactions associated with anesthesia. Concentrations of reduced glutathione were measured in the blood, liver, lung and kidney of the mouse after anesthesia with enflurane, fluroxene, halothane, isoflurane, methoxyflurane, or trichloroethylene. The anesthetic had no effect on glutathione concentrations in tissue except when fluroxene was used. After two hours of fluroxene anesthesia, glutathione in liver, lung, kidney, and blood was depleted by 93, 85, 85, and 61 per cent, respectively. The depletion was dose-dependent and was more extensive in animals anesthetized after phenobarbital pretreatment. Glutathione was also depleted in livers and lungs of rats anesthetized with ...
Researchers previous finding of a glutathione (GSH) deficiency in aging or senescent mice suggested that a concomitant decrease in detoxification capacity also may occur. To test this, mice at different biological stages of the life span (growth, maturity, aging or senescence) were injected with various doses of acetaminophen (APAP), and GSH depletion and recovery rates were determined. At intervals for 24 hr, samples of blood and other tissues were obtained, processed, and analyzed for reduced GSH, glutathione disulfide (GSSG), cysteine, and cystine using HPLC with dual electrochemical detection ...
TY - JOUR. T1 - Redox control of the transsulfuration and glutathione biosynthesis pathways.. AU - Deplancke, Bart. AU - Gaskins, H. Rex. PY - 2002/1. Y1 - 2002/1. N2 - Intracellular reduction-oxidation status is increasingly recognized as a primary regulator of cellular growth and development. The relative reduction-oxidation state of the cell depends primarily on the precise balance between concentrations of reactive oxygen species and the cysteine-dependent antioxidant thiol buffers glutathione and thioredoxin, which by preferentially reacting with reactive oxygen species, protect other intracellular molecules from oxidative damage. The transsulfuration pathway constitutes the major route of cysteine biosynthesis, and may thus be central in controlling the intracellular reduction-oxidation state and the balance between self-renewal and differentiation programs. This review discusses new findings on reciprocal reduction-oxidation modulation of enzymes involved in the transsulfuration and ...

Buthionine Sulfoximine | Harvard Catalyst Profiles | Harvard CatalystButhionine Sulfoximine | Harvard Catalyst Profiles | Harvard Catalyst

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Buthionine sulfoximine (BSO) is a sulfoximine which reduces levels of glutathione and is being investigated as an adjunct with ... Buthionine sulfoximine may also be used to increase the sensitivity of parasites to oxidative antiparasitic drugs. Defty, CL; ... "Definition of buthionine sulfoximine - National Cancer Institute Drug Dictionary". ...
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The Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa | IOVS | ARVO JournalsThe Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa | IOVS | ARVO Journals

Purpose: : We have administered Buthionine sulfoximine (BSO) an inhibitor of gamma-glutamylcysteine synthetase to wild type and ... The Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa ... The Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa ... The Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. ...
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Differential effects of l -buthionine sulfoximine and ethacrynic acid on glutathione levels and mitochondrial function in PC12...Differential effects of l -buthionine sulfoximine and ethacrynic acid on glutathione levels and mitochondrial function in PC12...

... buthionine sulfoximine and ethacrynic acid on glutathione levels and mitochondrial function in PC12 cells, Neuroscience Letters ... Differential effects of l -buthionine sulfoximine and ethacrynic acid on glutathione levels and... Seyfried, J.; Soldner, F.; ... Differential effects of l -buthionine sulfoximine and ethacrynic acid on glutathione levels and mitochondrial function in PC12 ... Differential effects of l -buthionine sulfoximine and ethacrynic acid on glutathione levels and mitochondrial function in PC12 ...
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The responses of Ht22 cells to oxidative stress induced by buthionine sulfoximine (BSO) | BMC Neuroscience | Full TextThe responses of Ht22 cells to oxidative stress induced by buthionine sulfoximine (BSO) | BMC Neuroscience | Full Text

in this study, GSH was depleted by inhibition of glutamylcysteine synthetase using buthionine sulfoximine (BSO) treatment in ... Seyfried J, Soldner F, Schulz JB, Klockgether T, Kovar KA, Wullner U: Differential effects of L-buthionine sulfoximine and ... in this study, GSH was depleted by inhibition of glutamylcysteine synthetase using buthionine sulfoximine (BSO) treatment in ... The responses of Ht22 cells to oxidative stress induced by buthionine sulfoximine (BSO). ...
more infohttps://bmcneurosci.biomedcentral.com/articles/10.1186/1471-2202-6-10

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Cytotoxic effects of glutathione synthesis inhibition by L-buthionine-(SR)-sulfoximine on human and murine tumor cells -...Cytotoxic effects of glutathione synthesis inhibition by L-buthionine-(SR)-sulfoximine on human and murine tumor cells -...

... buthionine sulfoximine (BSO) was tested for cytotoxicity and thiol depletion in murine and human tumor cells in vitro, and for ... Nifurtimox Is Effective Against Neural Tumor Cells and Is Synergistic with Buthionine Sulfoximine. *Michael Du, Linna Zhang, ... Glutathione depletion in tissues after administration of buthionine sulphoximine.. *Andrew Ivor Minchinton, Alain Rojas, +4 ... Cytotoxic effects of glutathione synthesis inhibition by L-buthionine-(SR)-sulfoximine on human and murine tumor cells. @ ...
more infohttps://www.semanticscholar.org/paper/Cytotoxic-effects-of-glutathione-synthesis-by-on-Dorr-Liddil/38ccf46fee048b565758df82b3cd9350d59fe61a

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Buthionine sulfoximine (BSO) was prepared at 50 mg/ml in water and administered by i.p. injection at 0.9 g/kg (18 ml/kg). After ... buthionine sulfoximine. ERK. extracellular signal-regulated kinase. GCL. glutamate cysteine ligase. GSSG. glutathione disulfide ... Administration of APAP and Buthionine Sulfoximine.. APAP was prepared as a 15-mg/ml suspension in phosphate-buffered saline ( ...
more infohttp://jpet.aspetjournals.org/content/355/2/137

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Patent US6359004 - Manipulating nitrosative stress to upregulate nitrosative stress defenses - Google PatentsPatent US6359004 - Manipulating nitrosative stress to upregulate nitrosative stress defenses - Google Patents

... mammals are treated for protozoal infections by systemic administration of L-buthionine-S-sulfoximine and agent that increases ... Novel agents include α-alkyl-S-alkyl-homocysteine sulfoximines wherein the α-alkyl contains 2 to 8 carbon atoms, and the S- ... α-propyl-DL-buthionine-SR-sulfoximine, α-isopropyl-DL-buthionine-SR-sulfoximine, α-butyl-DL-buthionine-SR-sulfoximine, α-tert ... α-propyl-buthionine sulfoximine, α-isopropyl-buthionine sulfoximine, and α-tert butyl-buthionine sulfoximine. ...
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Figure 1: Diethyl maleate (DEM) exposure causes an increase, while buthionine sulfoximine (BSO) exposure causes a decrease, in ... Diethyl maleate (DEM) directly conjugates to GSH while buthionine sulfoximine (BSO) inhibits γ-glutamylcysteine synthetase ... L-buthionine-sulfoximine (L-BSO), and diethyl maleate (DEM). Both compounds caused significant concentration and time dependent ...
more infohttps://www.hindawi.com/journals/omcl/2015/269371/

Effect of nonprotein thiols on protein synthesis in isolated rat hepatocytes | SpringerLinkEffect of nonprotein thiols on protein synthesis in isolated rat hepatocytes | SpringerLink

Glutahione depletion, induced by in vivod administration of L-buthionine sulfoximine and diethylmaleate, did not alter the ...
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Buthionine sulfoximine (GSH inhibition, hypertension) * 10. Multi-Factor Approach Cocaine + xanthine + xanthine oxidase + ...
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Buthionine sulfoximine View Synonyms. View Structure. Description:. A synthetic amino acid that depletes glutathione by ...
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Although the glutathione synthesis inhibitor buthionine sulfoximine potentiated the effect of doxorubicin and H2O2, the ...
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l-buthionine-sulfoximine. dox. doxycycline. ER. estrogen receptor. EV. empty vector. HMEC. human MEC. Luc. luciferase. MaSC. ... COMMA-1D cells were treated with l-buthionine-sulfoximine (BSO), a specific inhibitor of glutathione synthesis (Griffith, 1999 ...
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Buthionine sulfoximine pretreatment also increased the number of camptothecin-induced DNA-protein cross-links, indicating that ... Griffith, O. W. l-Buthionine-S,R-sulfoximine: mechanism of action, resolution of diastereomers and use as a chemotherapeutic ... Sawyer, T. E., and Bonner, J. A. The interaction of buthionine sulphoximine (BSO) and the topoisomerase I inhibitor CPT-11. Br ... 3 The abbreviations used are: topo, topoisomerase; BSO, buthionine sulfoximine; CGMMDC, 7-(cysteinylglycylmethyl)-10,11- ...
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Full text] Differential cytotoxic and radiosensitizing effects of silver nanopart | IJNFull text] Differential cytotoxic and radiosensitizing effects of silver nanopart | IJN

Abbreviations: AgNP, silver nanoparticle; GSH, glutathione; TNBC, triple-negative breast cancer; BSO, buthionine sulfoximine; ... or complete media with buthionine sulfoximine (BSO) (Sigma-Aldrich, St Louis, MO, USA). Cells were incubated overnight, and ...
more infohttps://www.dovepress.com/differential-cytotoxic-and-radiosensitizing-effects-of-silver-nanopart-peer-reviewed-fulltext-article-IJN

Chemotherapy in Treating Children With NeuroblastomaChemotherapy in Treating Children With Neuroblastoma

PILOT STUDY OF BUTHIONINE SULFOXIMINE (BSO) IN COMBINATION WITH MELPHALAN FOR HIGH RISK NEUROBLASTOMA PATIENTS. Trial Phase:. ... reasons may receive buthionine sulfoximine alone. PRIOR CONCURRENT THERAPY: At least 6 months since myeloablative therapy with ... PILOT STUDY OF BUTHIONINE SULFOXIMINE (BSO) IN COMBINATION WITH MELPHALAN FOR HIGH RISK NEUROBLASTOMA PATIENTS ... OBJECTIVES: I. Describe the toxic effects of combined chemotherapy with buthionine. sulfoximine (BSO) and melphalan (L-PAM) in ...
more infohttp://www.knowcancer.com/cancer-trials/NCT00002730/

Visualization of three-way comparisons of omics data | BMC Bioinformatics | Full TextVisualization of three-way comparisons of omics data | BMC Bioinformatics | Full Text

... buthionine sulfoximine (BSO), an inhibitor of γ-glutamylcysteine synthase. The plotted datasets are averages of five normalized ...
more infohttps://bmcbioinformatics.biomedcentral.com/articles/10.1186/1471-2105-8-72

Melphalan (Intravenous route)Melphalan (Intravenous route)

Buthionine Sulfoximine *Nalidixic Acid. Other interactions Certain medicines should not be used at or around the time of eating ...
more infohttps://www.allinahealth.org/CCS/doc/Thomson%20Detailed%20Drugs/47/602607.htm

Application # 2012/0035268. SPHINGO-GUANIDINES AND THEIR USE AS INHIBITORS OF SPHINGOSINE KINASE - Patents.comApplication # 2012/0035268. SPHINGO-GUANIDINES AND THEIR USE AS INHIBITORS OF SPHINGOSINE KINASE - Patents.com

... buthionine sulfoximine; calcipotriol; calphostin C; camptothecin derivatives; canarypox IL-2; capecitabine; carboxamide amino ...
more infohttp://patents.com/us-20120035268.html
  • Treatment with 500 μ M l -buthionine sulfoximine (BSO), which inhibits GSH synthesis, reduced cellular GSH but did not lead to generation of ROI. (deepdyve.com)
  • Buthionine sulfoximine may also be used to increase the sensitivity of parasites to oxidative antiparasitic drugs. (wikipedia.org)
  • This graph shows the total number of publications written about "Buthionine Sulfoximine" by people in Harvard Catalyst Profiles by year, and whether "Buthionine Sulfoximine" was a major or minor topic of these publication. (harvard.edu)
  • Below are the most recent publications written about "Buthionine Sulfoximine" by people in Profiles. (harvard.edu)