Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adriamycin treatment in vivo or addition to incubation mixtures in vitro inhibits hepatic drug metabolism. It has been suggested that adriamycin-induced membrane lipid peroxidation may be a mechanism responsible for this activity in vitro. To determine if similar mechanisms operate in vivo, adriamycin inhibition of drug metabolism was compared in rats whose tissue lipid peroxidizability was altered by manipulating dietary levels of vitamin E. Weanling rats maintained on vitamin E deficient (0 ppm) or supplemented (10 or 100 ppm) diets for 12 weeks were given either adriamycin, 5 mg/kg/week, or equal volumes of the saline vehicle for 3 weeks intraperitoneally. Vitamin E deficiency alone (0 ppm, saline pretreatment) produced a 37% increase in hepatic lipid peroxidation without any appreciable alteration in hepatic aniline hydroxylase, ethylmorphine N-demethylase or aryl hydrocarbon hydroxylase activities. Adriamycin pretreatment altered hepatic lipid peroxidizability over corresponding saline pretreated controls dependent on dietary vitamin E. No increase was seen in the 100 ppm group, while 44% and 500% increases occurred at 10 and 0 ppm vitamin E, respectively. Adriamycin pretreatment decreased drug-metabolizing enzyme activity by an average of 32% for aniline hydroxylase, 26% for ethylmorphine N-demethylase and 63% for aryl hydrocarbon hydroxylase. Statistically, decreases in drug metabolism were independent of dietary vitamin E and did not correlate with lipid peroxidizability. These data would suggest that in vivo adriamycin-induced depression of hepatic drug-metabolizing enzymes is not mediated by elevated lipid peroxidation.
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PMID:Increasing lipid peroxidation by vitamin E deficiency does not augment adriamycin-induced inhibition of hepatic drug metabolism. 665 95

Two experiments were conducted in aquaria to determine the minimum dietary selenium requirement of fingerling channel catfish (Ictalurus punctatus). Casein-gelatin diets containing graded levels of supplemental selenium (as Na2SeO3) ranging from 0 to 15 mg/kg were fed to catfish for 15 weeks in experiment 1 to broadly define their selenium requirement and toxicity levels. Although growth of catfish was affected by dietary selenium level, significant differences in weight gain were not easily discernible due to variability among the groups of fish. Weight gain data generally indicated that the basal diet containing 0.06 mg Se/kg diet caused growth depression, and a supplemental selenium level of 15 mg/kg also caused a reduced growth response, which indicated selenium toxicity. Selenium concentrations in edible muscle tissue increased almost linearly with increasing dietary selenium levels. Liver and plasma selenium-dependent glutathione peroxidase (Se GSH-Px) activities indicated the selenium requirement of fingerling channel catfish was between 0.1 and 0.5 mg Se/kg diet. In experiment 2, casein-gelatin diets containing incremental levels of supplemental selenium were fed to catfish for 14 weeks to more precisely determine their minimum dietary selenium requirement. Growth data and liver and plasma Se GSH-Px activities indicated that the minimum selenium requirement of fingerling channel catfish fed adequate vitamin E was 0.25 mg Se/kg dry diet. Based on these data, it appears that selenium supplementation of commercial catfish feeds is warranted.
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PMID:Dietary selenium requirement of fingerling channel catfish. 669 43

The interrelationships of dietary vitamin E and essential fatty acids and their effects on serum and pulmonary prostaglandin (PG) synthesis and fatty acid precursors were examined. In a preexperimental period, male weanling rats were depleted of essential fatty acids (EFA) by feeding on a hydrogenated coconut oil diet. At the end of 45 days, average serum triene:tetraene ratio for the EFA-deficient rats was 0.76. After a refeeding period with a 20% safflower oil diet and 0, 1 or 50 mg of dl-alpha-tocopheryl acetate daily, serum and pulmonary fatty acid profiles and PG synthesis were determined. A trend to growth depression on the high vitamin E diet was observed. Vitamin E supplementation seemed to have no significant effect on fatty acid composition or synthesis of PGE1, PGE2, PGF2 alpha or PGI2 in lung. This may be due to the small lipid content and presumed inability of lung to accumulate excess vitamin E. Lung may, therefore, be resistant to such dietary manipulations. Serum PG synthesis was not affected by vitamin E dose, although the C20:4 omega 6/C18:2 omega 6 ratio in serum was significantly lowered on the high vitamin E diet.
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PMID:Effects of dietary vitamin E on serum and pulmonary fatty acids and prostaglandins in rats fed excess linoleic acid. 672 76

Adjuvant arthritis was induced in rats fed a diet deficient in or supplemented with vitamin E, and its severity was scored according to the macroscopic findings of their legs, tails, and ears. The average score so obtained was higher in the vitamin E-deficient diet group than in the group of rats supplemented with vitamin E. Whereas the A/G ratio remained depressed in vitamin E-deficient rats, rats on a vitamin E-supplemented diet showed a fast recovery from A/G-ratio depression. The serum levels of beta-glucuronidase and acid phosphatase were elevated after administration of an adjuvant. The serum levels of these lysosomal enzymes showed a remarkable increase in rats fed a vitamin E-deficient diet, while the elevation in lysosomal enzyme levels in rats fed a vitamin E-supplemented diet was inhibited. The levels of thiobarbituric acid (TBA) reactants in the synovia were elevated at 2 weeks after exposure to the adjuvant and were decreased thereafter. In rats maintained on a diet supplemented with vitamin E, on the other hand, the increase in synovial level of TBA reactive substances was inhibited. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation and that antioxidants, such as vitamin E, may be beneficial for arthritis.
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PMID:Effect of vitamin E on adjuvant arthritis in rats. 686 Mar 21

Male rats were fed vitamin E-adequate, Torula yeast-based diets for 30 days to assess the influence of dietary selenium (0, 0.1, or 1.0 ppm) on the toxicity of dietary cadmium (0, 30, or 60 ppm). At all selenium levels, increased cadmium intake depressed feed consumption, reduced feed efficiency and lowered body weight gain. In liver, concentrations of cadmium and zinc increased, and iron concentration decreased with increased intake of cadmium. Dietary selenium did not affect concentrations of cadmium, zinc, iron or copper in liver. Blood hemoglobin level declined and relative heart weight (g/100 g body wt) increased with increased intake of cadmium. Increased selenium intake partially alleviated the cadmium-induced depression in blood hemoglobin levels in rats fed diets that contained 30 ppm cadmium, and partially ameliorated the cadmium-induced increase in heart size in rats fed either 30 or 60 ppm cadmium. Hepatic and renal glutathione peroxidase (GSH-Px) activity increased with increased selenium intake. Increased cadmium intake did not affect renal GSH-Px activity. Hepatic GSH-Px activity in rats fed diets that contained 0.1 ppm selenium decreased with increased cadmium intake; however, hepatic GSH-Px activity was not affected by dietary cadmium in rats fed diets that contained 1.0 ppm selenium. Interactions between nontoxic levels of dietary selenium and relatively high levels of dietary cadmium apparently resulted in an antagonism of selenium metabolism by cadmium in some systems, and partial amelioration of cadmium toxicity by selenium in other systems
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PMID:Some metabolic interrelationships between toxic levels of cadmium and nontoxic levels of selenium fed to rats. 707 26

Serum levels of alpha-tocopherol (vitamin E) were determined in various types of liver diseases, and as a results, it was revealed that serum alpha-tocopherol was significantly depressed in acute hepatitis (p less than 0.01, n = 22), alcoholic hepatitis (p less than 0.001, n = 9) and fulminant hepatitis (p less than 0.001, n = 6). There was a significant correlation between serum levels of alpha-tocopherol and beta-lipoprotein (r = 0.92, p less than 0.001, n = 17). Though there was no correlation between serum levels of alpha-tocopherol and triglyceride, there was a significant correlation between alpha-tocopherol and cholesterol (r = 0.57, p less than 0.01, n = 21), and phospholipid (r = 0.49, p less than 0.05, n = 18). There was no correlation between serum levels of alpha-tocopherol and other liver function tests. These facts suggested that the diminished serum vitamin E in patients with liver diseases is ascribable to the depression in blood level of beta-lipoprotein that results from liver disorders, because the liver is the major supply source of beta-lipoprotein.
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PMID:alpha-Tocopherol level in liver diseases. 715 92

In 3 experiments, 45 castrated male weanling pigs (4 to 6 weeks old) were used to determine the hematologic alterations induced by adriamycin (ADR) given IV at 0.64, 1.6, or 3.2 mg/kg of body weight/week. The effect of selenium-vitamin E (Se-E) supplements on ADR toxicosis was evaluated. Mortality, decreased survival time, growth depression, leukopenia, and anemia were dose related in ADR-treated pigs. At 0.64 mg of ADR/kg/week for 16 weeks, important clinical or hematologic alterations did not develop. At 1.6 mg of ADR/kg/week for 13 weeks, mortality was 100%, mean survival time ws 65.7 days (min-max, 49 to 92 days), and moderate growth depression and marked leukopenia and anemia were present from weeks 7 to 13. At 3.2 mg of ADR/kg/week for 4 weeks, mortality was 100% and mean survival time was 22.0 days (min-max, 18 to 26 days); marked growth depression, leukopenia, and mild anemia developed (week 4). Cytologic study of smears of bone marrow from pigs that died of ADR toxicosis (3.2 mg/kg/week) revealed marked hypoplasia and evidence of decreased production and increased destruction of erythroid and myeloid cells. Beneficial effect of Se-E supplementation against ADR toxicosis was seen only in the pigs given 1.6 mg/kg/week, where prolonged survival and delayed onset of leukopenia and anemia was observed.
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PMID:Effect of selenium-vitamin E on hematologic alterations of adriamycin toxicosis in young pigs. 727 Oct 34

The effect of megadoses of vitamin E was studied in 13 adult males and five young boys. Three hundred milligrams of vitamin E as dl-alpha-tocopheryl acetate, given daily for a period of 3 weeks produced a significant depression in the bactericidal activity of the leukocyte and the mitogen induced lymphocyte transformation. The delayed hypersensitivity of the skin to phytohemagglutinin was, however, not affected by the supplementation. The implication of the study and the discrepancy between the in vitro and the in vivo results of the cell-mediated immunity are discussed.
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PMID:Effect of vitamin E supplementation on leukocyte function. 735 45

Lungs accumulate 5-hydroxytryptamine (serotonin, 5-HT) from the perfusate by a sodium-dependent, energy-requiring, saturable process. The rate-limiting step for uptake is the transport of 5-HT and not its subsequent metabolism to 5-hydroxyindoleacetic acid. Autoradiographic studies indicate that the pulmonary endothelium is the cellular site of uptake. The effect of hyperoxia on lung clearance of 5-HT was studied with isolated perfused and ventilated lungs from rats that were previously exposed to hyperoxia. Lungs were perfused with recirculating electrolyte solution and initial [5-HT] of 0.24 microM. The calculated fractional 5-HT clearance (fracion of 5-HT removed in a single pass) ws 0.77 +/- 0.02 (mean +/- SE: n = 44) for control rats. Mean fractional clearance decreased by 20% in rats exposed to 1 atm O2 for 18 hr and 30% after 4 atmospheres absolute (ata) O2 for 1 hr (p < 0.05). The effects of O2 at 4 ata were in part reversed by exposure to air for 3.5 hr and in part prevented by injection of superoxide dismutase (60 nmole/kg body weight). This degree of O2 exposure at either 1 or 4 ata had no effect on lung content of adenine nucleotides or the distribution of 3H-5HT on autoradiography. Rats maintained for 6 weeks on a vitamin E-deficient diet showed an increased effect of hyperoxia on 5-HT clearance and did not show reversal of changes after 24 hr of air breathing. The results indicate that exposure to elevatd po2 results in reversible depression of pulmonary 5-HT clearance that is potentiated by vitamin E deficiency. This suggests alteration of pulmonary endothelial membrane transport properties due to O2 toxicity.
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PMID:Environmental influences on uptake of serotonin and other amines. 740 97

A corn-soybean (CS) diet and diets containing medium or high levels of animal protein (AP) calculated to contain the same concentrations of the main nutrients promoted essentially the same growth rate and feed utilization in 20-day-old chicks. Supplementation with monensin sodium (100 or 120 mg/kg) depressed growth rate of the chicks fed all three diets. However, effect of the drug was much more severe in chicks fed the diets containing AP. This interaction resulted in significant (P < .05) differences in body weights between chicks fed the CS diet and PA diets. Moreover, feed-to-gain ratio was significantly (P < .05) adversely affected by monensin only in chicks fed the AP diets. Supplementation of the high AP diet with extra vitamin E, a mixture of arginine and tryptophan, or a mixture of silicon, chromium, and molybdenum failed to prevent the growth depression caused by monensin. These studies demonstrate that ingredient composition of diets for broiler chicks affects the magnitude of growth depression caused by monensin supplementation.
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PMID:Effect of dietary ingredients on monensin toxicity in chicks. 741 86


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