Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: DrugBank:EXPT03226 (vitamin E)
 17,558 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin synthetase activity in high-speed particulate fractions of chick epiphyseal cartilage has been characterized with respect to cofactor requirements, pH optimum, buffer-ion effects, types of prostaglandins formed, and the distribution of prostaglandin synthetase activity in zones of the epiphyseal plate. Direct homogenization of cartilage was found to be more efficacious than releasing chondrocytes by enzymatic digestion for preparation of prostaglandin synthetase, a homogenization time of 4 min yielding maximal activity. The optimal incubation medium contained 50 mM Tris buffer (pH 7.5), 2.5 mM epinephrine, 1 micronM hemoglobin, 3.25 mM glutathione, 200 microgram/ml enzyme protein, and 5 micronM substrate. Glutathione was effective only if present during homogenization. Rates of PGE2 biosynthesis were linear up to 15 min and then rapidly declined, indicative of self-deactivation. The low levels of PGF2alpha formed, and their decrease after 20 min incubation, suggests the possible presence of degradative enzymes. Prostaglandin synthetase was inhibited by aspirin, indomethacin, and vitamin E, but not vitamin K1. Cation concentrations in the physiological range had only modest effects on prostaglandin biosynthesis, and then only if present during tissue homogenization. In the presence of phosphate buffer, Ca2+ was somewhat inhibitory. Since in the absence of phosphate Ca2+ had no deleterious effect, it is probably that the inhibitory effect was caused by precipitation of calcium phosphate. Hypertrophic and calcified cartilage exhibited significantly higher prostaglandin synthetase activity than the proliferating and maturing zones. The increased synthesis of prostaglandins in the low layers of the growth plate may indicate a role of these factors in chondrocyte differentiation and/or calcification.
 ...
PMID:Localization of prostaglandin synthetase in chicken epiphyseal cartilage. 10 4

Liposomes were prepared from phospholipids extracted from biological membranes. A comparison was made between the peroxidation rate in handshake liposomes and in sonicated liposomes. The smaller sonicated liposomes were more vulnerable to peroxidation, probably because of the smaller radius of curvature, which results in a less dense packing of lipid molecules in the bilayer and a facilitated action of water radicals produced by the X-irradiation. High oxygen enhancement ratios were obtained, especially at low dose rates, suggesting the operation of slowly progressing chain reactions initiated by ionizing radiation. Three compounds were tested for their ability to protect the liposomal membranes against lipid peroxidation. The naturally occurring compounds reduced glutathione (GSH) and vitamin E(alpha-T) and the powerful radiation protector cysteamine (MEA). All three molecules could protect the liposomes against peroxidation. The membrane-soluble compound vitamin E was by far the most powerful. About 50 per cent protection was achieved by using 5 X 10(-6) M alpha-T, 10(-4) M GSH and 5 X 10(-4) M MEA. The fatty acid composition of the lipids altered drastically as a result of the irradiation. Arachidonic acid and docosahexanoic acid were the most vulnerable of the fatty acids. Very efficient protection of these polyunsaturated fatty acids could be obtained with relatively low concentrations of vitamin E built into the membranes.
 ...
PMID:Protection of liposomal lipids against radiation induced oxidative damage. 31 91

Neutrophils and monocytes are the prime defenders of the body against suppurative bacterial and fungal infections. To accomplish their role in inflammation, they must respond appropriately to chemotactic signals elaborated from complement and bacteria. This response predictably results in the adherence and subsequent directed movement of the phagocytes toward the infected area where they recognize opsonized microbes. Attachment of the microbes to the membrane of the cell leads to their ingestion and subsequent demise, principally by the reduced oxygen by-product H2O2, which is generated by the neutrophils and monocytes during phagocytosis. Optimal killing requires the translocation of granule myeloperoxidase into the phagocytic vacuole containing the bacteria and a suitable halide ion. Degranulation is controlled, in part, by assembled microtubules whereas ingestion requires assembly of submembrane microfilaments. Deficiency states resulting from vitamin E results in diminished membrane-related chemotaxis and ingestion, whereas depletion of cellular GSH results in defective microtubule assembly preventing the normal increase in adherence, chemotaxis, degranulation, and microbicidal activity of the phagocytic cells. Deficiency states resulting in dysfunction of the microtubule system include neutrophil glutathione synthetase deficiency, rodent glutathione peroxidase deficiency, and the Chediak-Higashi syndrome.
 ...
PMID:Role of membrane vitamin E and cytoplasmic glutathione in the regulation of phagocytic functions of neutrophils and monocytes. 39 94

The effects of various levels of selenium, alpha-tocopherol and sulfur on glutathione peroxidase (GSH-Px) activity in intestinal and liver tissues were determined in male rats fed corn-soybean or Torula yeast diets. Rats fed corn-soybean diets had greater GSH-Px activity in the small intestine, colon and liver tissues, catalase activity and selenium in the liver, and body weight gains than those fed Torula yeast diets. GSH-Px activity in the small intestine, colon, and liver tissues as well as concentration of selenium in the liver increased with increasing levels of selenium in Torula yeast diets but not with corn-soybean diets. Tocopherol supplementation had no significant effect on GSH-Px activity in rats fed Torula yeast or corn-soybean diets supplemented with selenium. Supplemental sulfur decreased GSH-Px activity in the small intestine tissues and increased activity in colon tissues.
 ...
PMID:Glutathione peroxidase acitvity in intestinal and liver tissues of rats fed various levels of selenium, sulfur and alpha-tocopherol. 43 Feb 45

Two groups of weanling male Hartley guinea pigs maintained on vitamin E deficient diet were supplemented with 0.4 I.U./100 g body weight/day of vitamin E and either 2 (Group A) or 10 (Group B) mg/100 g body weight/day of vitamin C for 5 weeks. As compared to Group A, the degree of erythrocyte hemolysis and liver TBAR level of Group B were significantly increased while plasma vitamin E and erythrocyte GSH levels were significantly decreased. In another experiment, two groups of guinea pigs were given 0.8 I.U./100 g body weight/day of vitamin E and 2 (Group C) or 30 mg/100 g body weight/day (Group D) of vitamin C. Levels of plasma vitamin E and erythrocyte GSH of Group D were significantly lower than those of Group C: however, erythrocyte hemolysis and liver TBAR were not affected by the level of vitamin C supplementation. The results suggest that the high levels of vitamin C supplementation lowered tissue antioxidant potential of animal when vitamin E was marginally adequate, and the hemolytic and peroxidizing effect of high level of vitamin C may be counteracted by increasing the level of vitamin E.
 ...
PMID:Effects of high level of vitamin C on tissue antioxidant status of guinea pigs. 44 55

The effect of dietary selenium and vitamin E on the important cellular antioxidant defense systems was studied in rat erythrocytes. Weanling male Sprague-Dawley rats were fed a basal selenium and vitamin E deficient diet and supplemented with either none or 0.5 ppm selenium and either none or 45 ppm vitamin E for 35 or 40 days. Depletion of dietary selenium resulted in marked decrease of glutathione (GSH) peroxidase in the red cells, but the levels of GSH, catalase and superoxide dismutase were not significantly altered. The red cells of rats fed the basal diet deficient in both selenium and vitamin E had significantly lower levels of GSH and GSH peroxidase, but not of catalase and superoxide dismutase, than in those fed the basal diet and supplemented with either selenium, vitamin E or both. The results suggest that depletion of dietary selenium and vitamin may have a precipitate effect on lowering the levels of GSH and GSH peroxidase in rat erytyrocytes.
 ...
PMID:Effect of dietary selenium and vitamin E on the antioxiant defense systems of rat erythrocytes. 46 73

Weanling male Sprague-Dawley rats were fed either a synthetic diet supplemented with 11 mg vitamin E/kg body weight (to approximate average U.S. human dietary intake) or a commercial rat chow for 5 wk. At 2 months of age, rats were exposed to either 0.0, 0.1, or 0.2 ppm ozone continuously for 7 days. Morphological lesions were consistently present in centriacinar regions of lungs of both groups of rats at the 0.2 ppm level. At 0.1 ppm ozone, two of six rats fed the synthetic diet and two of five fed lab chow had minimal centriacinar lesions. Biochemical assays showeed that the activities of glutathione (GSH) peroxidase, GSH reductase, and G-6-P dehydrogenase and level of nonprotein sulfhydryls in the lungs of rats fed the synthetic diet and exposed to 0.1 ppm were elevated to about one-half the level that was produced by 0.2 ppm. The authors conclude that the level whereby there are no observable morphologic effects for short-term exposure to ozone in 2-month-old rats is less than, but close to, 0.1 ppm.
 ...
PMID:Pulmonary alterations in rats exposed to 0.2 and 0.1 ppm ozone: a correlated morphological and biochemical study. 51 18

Thirty-two adult female white-tailed deer were assigned to four complete pelleted diets (+/- 45 ppm vitamin E; +/- 0.2 ppm selenium). Selenium and vitamin E concentration in the unsupplemented diet was 0.04 and 5.5 ppm, respectively. Biochemical parameters of the erythrocyte (RBC) glutathione peroxidase system and survival of off-spring to weaning were followed for 2 years. At the end of the second year, 12 male young (3 per treatment) and the remaining adults were killed, and liver and muscle parameters of the glutathione system determined. Plasma selenium (Se) and vitamin E (E) were significantly lower among unsupplemented adults within 6 months of treatment and remained essentially constant from 10 months on. In vitro hemolysis and mortality of young were affected by dietary E but not by Se. Tissue glutathione peroxidase (GSH-Px) was correlated with tissue Se in all tissues measured (RBC, liver and muscle). Tissue Se, in turn, was related to dietary Se. Thus, dietary Se deficiency (Se = 0.04 ppm) resulted in biochemical deficiency (depressed GSH-Px). This was not reflected in gross lesions among the adults, nor in increased mortality among young.
 ...
PMID:The effect of dietary selenium and vitamin A on biochemical parameters and survival of young among white-tailed deer (Odocoileus virginianus). 56 48

Toxic doses of butylated hydroxytoluene (BHT), a phenolic antioxidant commonly used as a food additive, are known to produce lung damage. In this study, 3 days after a single ip injection of 62.5, 215, or 500 mg/kg BHT in mice there was a dose-dependent increase in lung weight. This concentration dependence with injected BHT was accompanied by increases in lung DNA and nonprotein sulfhydryl levels and in whole lung tissue enzyme activities of glutathione (GSH) peroxidase, GSH reductase, glucose-6-phosphate dehydrogenase, and superoxide dismutase. The increased enzyme activities are considered to correspond to inflammatory and proliferative pulmonary changes resulting from acute lung cell injury and necrosis, which have been described previously, and cannot be construed as evidence for a primary oxidant-induced pulmonary lesion. The mechanism of BHT-induced lung changes may not be related to the antioxidant property of BHT, since vitamin E, n-propyl gallate, ethoxyquin, N,N'-p-phenylenediamine, and the structurally similar compound, butylated hydroxyanisole did not appear to produce the gross anatomical or biochemical lung changes observed with BHT.
 ...
PMID:Effect of butylated hydroxytoluene and other antioxidants on mouse lung metabolism. 59 82

One hundred and twenty female mice fed diets containing various levels of vitamin E were continuously exposed to 0.5 ppm, 1.0 ppm nitrogen dioxide (NO2), and filtered air for 17 months. Blood, lung, and liver tissues were assayed for glutathione peroxidase (GSH-peroxidase) activity. Exposure to 0.5 ppm NO2 did not affect blood and lung GSH-peroxidase activity; 1.0 ppm NO2 exposure, however, caused suppression of the enzyme. A combination of vitamin E deficiency and 1.0 ppm NO2 exposure resulted in the lowest GSH-peroxidase activities in the blood and lung. High levels of vitamin E in the diet resulted in elevated GSH-peroxidase in the blood and lung. Liver GSH-peroxidase activity was unaffected by either dietary vitamin E or NO2 exposure. No inverse relationship was found between GSH-peroxidase levels and concentrations of organic solvent soluble lipofuscin pigments present in tissues.
 ...
PMID:Long-term NO2 exposure of mice in the presence and absence of vitamin E. II. Effect of glutathione peroxidase. 73 11


1 2 3 4 5 6 7 8 9 10 Next >>