Perinatal nephropathies. (1/1198)
The purpose of this paper is to review the development of the mammalian kidney and to assess the influence that various perinatal manipulations may have on the developmental process either morphologically or functionally. Immature kidneys in general have less functional capacity than adult kidneys and a low rate of glomerular filtration, perhaps related to renal blood flow, which appears to limit the disposition of a fluid or solute load. Tubular reabsorption is also limited leading to the urinary loss of glucose, amino acids, bicarbonate and phosphate. Although the relatively low function of the immature kidney is a normal part of development, its capacity to respond under conditions of stress may be less adequate than in adults. An additional concern is that a variety of perinatal manipulations, such as the incidental or accidental ingestion of a chemical, may lead to varying degrees of altered morphogenesis or functional development of the kidney. Chemical induced renal anomalies may be of several types, but in typical teratology experiments hydronephrosis may be the most frequent observation. The functional consequences of these renal malformations may be lethal or inconsequential or while an animal may be able to survive and develop normally in the presence of a renal malformation, it is possible that a stressful situation would unmask a functional malformation which could compromise survival. Thus, some renal abnormalities may be subtle enough to go unnoticed without experimental tests. Without such tests it is impossible to evaluate the effect of functional alterations on successful adaptation. (+info)Identification and characterization of an ascorbic acid transporter in human granulosa-lutein cells. (2/1198)
Ascorbic acid serves a vital role as a pre-eminent antioxidant. In animals, it has been shown to be concentrated in granulosa and theca cells of the follicle, in luteal cells of the corpus luteum, and in the peripheral cytoplasm of the oocyte. We have previously identified hormonally-regulated ascorbic acid transporters in rat granulosa and luteal cells, and herein present preliminary evidence for the presence of a transporter for ascorbic acid in human granulosa-lutein cells. Granulosa-lutein cells were obtained from the follicular fluid of patients undergoing in-vitro fertilization. Following an overnight incubation, the cells were incubated with [14C]-ascorbic acid (0.15 microCi; 150 microM) and ascorbic acid uptake was determined. The uptake of ascorbic acid was saturable with a Michaeli's constant (Km) and maximum velocity (Vmax) of 21 microM and 3 pmol/10(6) cells/min respectively. Ouabain, low Na+ medium, and dinitrophenol significantly inhibited ascorbic acid uptake (P<0.05). Neither the presence of insulin, human chorionic gonadotrophin (HCG), insulin-like growth factor (IGF)-I, nor IGF-II affected the uptake of ascorbic acid in a statistically significant fashion. Following saturation of cellular uptake, the ascorbic acid level was estimated to be 1.04 pmoles/10(6) cells or approximately 1 mM, a high concentration similar to that seen in rat luteal cells. Active ascorbic acid transport in human granulosa-lutein cells appears to occur via a Na+ - and energy-dependent transporter, with high levels of ascorbic acid being accumulated in these cells. (+info)Salivary histatin 5 induces non-lytic release of ATP from Candida albicans leading to cell death. (3/1198)
Salivary histatins are potent in vitro antifungal proteins and have promise as therapeutic agents against oral candidiasis. We performed pharmacological studies directed at understanding the biochemical basis of Hst 5 candidacidal activity. Three inhibitors of mitochondrial metabolism: carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5 killing of Candida albicans, while not inhibiting cellular ATP production. In contrast, Hst 5 caused a drastic reduction of C. albicans intracellular ATP content, which was a result of an efflux of ATP. Carbonyl cyanide p-chlorophenylhydrazone, dinitrophenol, and azide inhibited Hst 5-induced ATP efflux, thus establishing a correlation between ATP release and cell killing. Furthermore, C. albicans cells were respiring and had polarized membranes at least 80 min after ATP release, thus implying a non-lytic exit of cellular ATP in response to Hst 5. Based on evidence that transmembrane ATP efflux can occur in the absence of cytolysis through a channel-like pathway and that released ATP can act as a cytotoxic mediator by binding to membrane purinergic receptors, we evaluated whether extracellular ATP released by Hst 5 may have further functional role in cell killing. Consistent with this hypothesis, purinergic agonists BzATP and adenosine 5'O-(thiotriphosphate) induced loss of C. albicans cell viability and purinergic antagonists prevented Hst 5 killing. (+info)FcepsilonRI-mediated antigen endocytosis turns interferon-gamma-treated mouse mast cells from inefficient into potent antigen-presenting cells. (4/1198)
Previous studies in our laboratory have shown that bone-marrow-derived mast cells (BMMC) could present immunogenic peptides, from soluble antigens endocytosed through fluid phase, only if they were subjected to a 48-hr treatment with interleukin-4 (IL-4) and granulocyte-macrophage colony-stimulating factor (GM-CSF). In contrast to GM-CSF, interferon-gamma (IFN-gamma) which highly upregulates major histocompatibility complex (MHC) class II expression, completely inhibits the generation of immunogenic peptides. We have used this model to study the role of FcepsilonRI-mediated antigen internalization in the regulation of the antigen-presenting function of IFN-gamma-treated mast cells. Here, we report that FcepsilonRI can reverse the IFN-gamma-treated mast cells from inefficient to highly efficient antigen-presenting cells. Inhibition of the antigen presenting capacity by piceatannol, a protein tyrosine kinase (PTK) syk inhibitor, indicates that this is an active process resulting from immunoglobulin E (IgE)-antigen-FcepsilonRI engagement which involves tyrosines found in the immunoreceptor tyrosine-based activation motif (ITAM) embedded in the cytoplasmic tail of the FcepsilonRI beta and gamma chains. Antigen-presenting function was also shown to require the activation of phosphatidyl inositol 3 (PI3) kinase, downstream of PTK syk phosphorylation, since this activity was completely blocked by wortmannin, a PI3 kinase inhibitor. These data suggest that signalling generated by FcepsilonRI provides mast cells with IgE-mediated enhanced antigen presentation to T cells and emphasize a so far unknown immunoregulatory mast-cell function that might take place in inflammatory sites. (+info)Glutathione peptidomimetic drug modulator of multidrug resistance-associated protein. (5/1198)
The peptidomimetic drug gamma-glutamyl-S-(benzyl)cysteinyl-R-(-)-phenyl glycine diethyl ester (TER199) is an analog of glutathione designed to be an isozyme-specific inhibitor of GSTP1-1 protein1-1. This compound (and the de-esterified moiety) is shown to be an effective inhibitor of multidrug resistance-associated protein1 (MRP1)-mediated drug resistance. Kinetic analyses revealed that gamma-glutamyl-S-(benzyl)cysteinyl-R-(-)-phenyl glycine reversibly inhibits the transport of 2,4-dinitrophenyl-S-glutathione with a K(i) of 752 microM. TER199 reversed the accumulation deficit of daunorubicin in MRP1-transfected NIH3T3 fibroblasts and maintained intracellular levels for >2 h after daunorubicin removal. Cytotoxicity assays revealed that TER199 significantly reversed the resistance of MRP1-transfected NIH3T3 cells for vincristine, doxorubicin, etoposide, and mitoxantrone. HL-60 cells made resistant to TER199 by chronic, long-term selection had increased mRNA and protein levels of multidrug resistance-associated protein, MRP1, and gamma-glutamyl cysteine synthetase heavy and light subunits (the rate-limiting enzyme in GSH synthesis). In spite of increased gamma-glutamyl cysteine synthetase, their glutathione content was reduced approximately 35% from that of parental HL-60 cells. These cells also exhibited a drug resistance profile commensurate with the previously described MRP1 overexpressing phenotype, with resistance to Vinca alkaloids, epipodophyllotoxins, and anthracyclines; additional cross-resistance to paclitaxel (Taxol), mitoxantrone, and 5-fluorouracil was observed. (+info)Interaction of lymphocytes with lipid bilayer membranes: a model for lymphocyte-mediated lysis of target cells. (6/1198)
Horizontal lipid bilayer membranes were used as a model system to study lymphocyte-mediated killing of target cells. Dinitrophenylated lipid bilayers can physically support dozens of lymphocytes for periods of over one hour without breakage or increasing the electrical conductance of the membrane. However, in the presence of antibody against Dnp, human lymphocytes rapidly induced increases in membrane conductance of several orders of magnitude without membrane breakage. Such ionic permeability increases occurred only when the membrane voluage was positive on the lymphocyte side, as would be the case with a target cell membrane. The lymphocyte and antibody dependence of this conductance increase parallels that observed for lymphocyte killing of antibody-coated target cells. The results are interpreted as evidence that the primary event in lymphocyte killing of antibody-coated target cells is the creation of ion-conducting channels in the target membrane. (+info)Involvement of a phosphatidylinositol 3-kinase-p38 mitogen activated protein kinase pathway in antigen-induced IL-4 production in mast cells. (7/1198)
We studied the involvement of phosphatidylinositol 3-kinase (PI3-kinase) in the antigen-induced IL-4 production in a rat mast cell line, RBL-2H3. The stimulation of IgE-sensitized RBL-2H3 cells by the antigen resulted in increased IL-4 mRNA levels followed by increased IL-4 production. Wortmannin and LY294002, PI3-kinase inhibitors, partially reduced both the antigen-induced increases in the IL-4 mRNA levels and IL-4 production in a concentration-dependent manner. Extracellular signal-regulated kinase, p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK), which belong to the MAPK family, were activated by the antigen stimulation, and the activation of p38 MAPK in addition to JNK was suppressed markedly by wortmannin. The phosphorylation of endogenous activating transcription factor-2, a substrate of p38 MAPK, was also inhibited by wortmannin. The specific p38 MAPK inhibitor SB203580 partially inhibited the antigen-induced IL-4 production at mRNA levels, but the MEK-1 inhibitor PD98059 enhanced it. These findings suggest that the activation of PI3-kinase and p38 MAPK is partially responsible for the antigen-induced IL-4 production in RBL-2H3 cells. (+info)Cdc42 and Rac stimulate exocytosis of secretory granules by activating the IP(3)/calcium pathway in RBL-2H3 mast cells. (8/1198)
We have expressed dominant-active and dominant-negative forms of the Rho GTPases, Cdc42 and Rac, using vaccinia virus to evaluate the effects of these mutants on the signaling pathway leading to the degranulation of secretory granules in RBL-2H3 cells. Dominant-active Cdc42 and Rac enhance antigen-stimulated secretion by about twofold, whereas the dominant-negative mutants significantly inhibit secretion. Interestingly, treatment with the calcium ionophore, A23187, and the PKC activator, PMA, rescues the inhibited levels of secretion in cells expressing the dominant-negative mutants, implying that Cdc42 and Rac act upstream of the calcium influx pathway. Furthermore, cells expressing the dominant-active mutants exhibit elevated levels of antigen-stimulated IP(3) production, an amplified antigen-stimulated calcium response consisting of both calcium release from internal stores and influx from the extracellular medium, and an increase in aggregate formation of the IP(3) receptor. In contrast, cells expressing the dominant-negative mutants display the opposite phenotypes. Finally, we are able to detect an in vitro interaction between Cdc42 and PLCgamma1, the enzyme immediately upstream of IP(3) formation. Taken together, these findings implicate Cdc42 and Rac in regulating the exocytosis of secretory granules by stimulation of IP(3) formation and calcium mobilization upon antigen stimulation. (+info)Dinitrophenols (DNP) are a class of chemical compounds that contain two nitro groups (-NO2) attached to a phenol group. Dinitrophenols have been used in the past as industrial dyes, wood preservatives, and pesticides. However, they have also been misused as weight loss supplements due to their ability to increase metabolic rate and cause weight loss.
The use of DNP for weight loss is dangerous and has been linked to several fatalities. DNP works by disrupting the normal functioning of the mitochondria in cells, which are responsible for producing energy. This disruption causes an increase in metabolic rate, leading to a rapid breakdown of fat and carbohydrates, and ultimately weight loss. However, this increased metabolism can also produce excessive heat, leading to hyperthermia, dehydration, and damage to organs such as the heart, liver, and kidneys.
Due to their potential for serious harm, DNP-containing products are banned in many countries, including the United States. Medical professionals should be aware of the dangers associated with DNP use and advise patients accordingly.
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Levels of dinitrophenols5
- Swallowing low levels of dinitrophenols for short or long periods of time can cause an increase in heart and breathing rates, weight loss, a feeling of warmth, increase sweating, and possibly death. (cdc.gov)
- Cataracts, skin rashes, and fewer white blood cells in the blood were also seen in people who swallowed low levels of dinitrophenols. (cdc.gov)
- Tests are available to measure levels of dinitrophenols and its breakdown products in blood and urine. (cdc.gov)
- 2-amino-4-nitrophenol (predominant) and There are no recent monitoring data for for weight loss and body building by 4-amino-2-nitrophenol and then to levels of dinitrophenols in air. (cdc.gov)
- There are no recent monitoring data for excreted in the urine and, with profuse levels of dinitrophenols in drinking water. (cdc.gov)
Isomers2
- There are six isomers of dinitrophenol: 2,3-Dinitrophenol 2,4-Dinitrophenol 2,5-Dinitrophenol 2,6-Dinitrophenol 3,4-Dinitrophenol 3,5-Dinitrophenol Dinitrophenols also form the core structure of some herbicides, which are collectively referred to as dinitrophenol herbicides, including: Dinofenate Dinoprop Dinosam Dinoseb Dinoterb DNOC Etinofen Medinoterb Wikimedia Commons has media related to Dinitrophenols. (wikipedia.org)
- Dinitrophenols can be explosive when different dinitrophenol isomers are likely number of resorptions, stil born pups, dry. (cdc.gov)
512851
- Information profiles were presented for the following nitrophenols deemed important in the industrial community: 2-nitrophenol (88755), 3-nitrophenol (554847), 4-nitrophenol (100027), 2,4- dinitrophenol (51285), and 2,4,6-trinitrophenol (88891). (cdc.gov)
Sediment1
- Dinitrophenols will move onto sediment or suspended soil from water if the water is acidic and has lots of organic material. (cdc.gov)
Blood and urine1
- and metabolism of dinitrophenols is be measured in blood and urine. (cdc.gov)
Solids1
- Dinitrophenols can be either solids or gases in the air and may travel long distances through the air. (cdc.gov)
Groundwater2
Chemicals1
- Dinitrophenols are a class of manufactured chemicals that do not occur naturally in the environment. (cdc.gov)
Aqueous1
- An expanded graphite-carbon nanofiber-epoxy composite (EG-CNF-Epoxy) was investigated in order to its use for the electrochemical determination of 2,4-dinitrophenol (2,4-DNP) in aqueous solutions. (upt.ro)
Metabolism2
- 2,4-dinitrophenol (2,4-DNP) as sodium salt can cause effects on human and its metabolism, manifesting by high fever, high temperature, high respiratory rate and death, after acute, sub-acute and subchronic exposue. (europa.eu)
- 2,4-Dinitrophenol slowed the influx of only those compounds whose metabolism it blocks. (biologists.com)
MeSH1
- Dinitrophenols" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (musc.edu)
Soil1
- Dinitrophenols can be removed from the air into water or soil. (cdc.gov)
Supplements2
Acid2
Exposure2
Risks1
- In the 1930s 2,4-dinitrophenol was used in diet pills but was banned for this use in 1938 because of health risks. (cdc.gov)
Acute2
- No acute-duration oral MRL was derived for dinitrophenols. (cdc.gov)
- 2,4-dinitrophenol (DNP): a weight loss agent with significant acute toxicity and risk of death. (pneumotox.com)
Behavior1
- Cadmium behavior was similar, except for 2,4-dinitrophenol, where Cd sorption was increased. (epa.gov)
Dose1
- 1934) a dose of 7 mg of 2,4-dinitrophenol sodium salt (LOAEL) has been taken for 5 days by a woman. (europa.eu)
Chemical2
- Dinitrophenols are chemical compounds which are nitro derivatives of phenol. (wikipedia.org)
- Shiraishi, F, Miyawaki, A & Chand, R 2015, ' A mechanism of the photocatalytic decomposition of 2,4-dinitrophenol on TiO 2 immobilized on a glass surface ', Chemical Engineering Journal , vol. 262, pp. 831-838. (elsevierpure.com)
Weight loss3
- Studies in animals show that the most common effect of dinitrophenol is weight loss and increased body temperature. (cdc.gov)
- Deliberate poisoning with dinitrophenol (DNP): an unlicensed weight loss pill. (pneumotox.com)
- The pills contained 2,4-dinitrophenol (DNP), which is essentially an illegal weight loss aid. (theness.com)
Effects2
- Most of the information on health effects of dinitrophenols comes from old studies of patients who were prescribed diet pills containing dinitrophenol before it was banned. (cdc.gov)
- Dinitrophenol applies its effects in the cell, more specifically in the membrane of the mitochondria. (buysteroidtablets.com)
Water1
- If you live near a hazardous waste site, you might be exposed to dinitrophenols from contaminated air, water, or dirt. (cdc.gov)
Important1
- 2,4- Dinitrophenol was far more acutely toxic than other important nitrophenol derivatives. (cdc.gov)
Profile1
- Profile for Dinitrophenols. (cdc.gov)
Environment1
- What happens to dinitrophenols in the environment? (cdc.gov)
General2
People4
- Most people are not likely to be exposed to dinitrophenols. (cdc.gov)
- Most people don't need to take any special steps to avoid dinitrophenols in their daily lives. (cdc.gov)
- This graph shows the total number of publications written about "Dinitrophenols" by people in this website by year, and whether "Dinitrophenols" was a major or minor topic of these publications. (musc.edu)
- Below are the most recent publications written about "Dinitrophenols" by people in Profiles. (musc.edu)
Yellow1
- Dinitrophenol is a chromotropic pH indicator that is colorless below pH 2.6 and yellow above pH 4.4. (mfa.org)
High1
- In the 1940s and earlier, factory workers who breathed or came in contact with high amounts of dinitrophenols for a short and long period of time experienced fever, sweating, restlessness, decreases in white blood cells, and sometimes death. (cdc.gov)
Potential1
- The Department of Health and Human Services, U.S. Environmental Protection Agency (EPA), and International Agency for Research on Cancer (IARC) have not evaluated the potential for dinitrophenols to cause cancer. (cdc.gov)
Groups1
- More minor groups of synthetic organic insecticides include the formamidines (e.g., amitraz, formeta-nate) and dinitrophenols (e.g., binapacryl, dinocap). (encyclopedia.com)
Data1
- Current data support earlier findings regarding the hazards of pesticides such as 2,4- DNP (Dinitrophenol) and fungicides. (ehcd.com)
Body1
- Dinitrophenols are used in the Dinitrophenols exist in both the vapor fetal/pup body weight and length. (cdc.gov)