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)

Sodium selenite was fed in the diet in concentrations of 3, 1 and 0.50 ppm to hybro-type chicks for 4 weeks from the age of 7 d. The chemical's effects on growth and tissues were investigated. One and 3 ppm dietary levels of selenium caused depression of growth, fatty change, focal necrosis, congestion of the sinusoids and slight fibroplasia in the liver, congestion and degeneration and/or necrosis of the cells of the proximal renal tubules and of the cardiac muscle fibers and hemorrhage in the thigh and breast. These changes were accompanied by an increase in the activity of sorbitol and glutamic dehydrogenases (SDH and GDH) and in the concentration of potassium, and a decrease in the levels of total protein, calcium and zinc in the serum. Susceptibility to hemorrhage and damage to kidneys and liver persisted for 3 weeks after the test diet was withdrawn. One-half of 1 ppm-selenite meal produced no adverse effects on the chicks.
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PMID:Effects of various levels of dietary selenium on hybro-type chicks. 370 35

Information concerning selenium status in thermal injury patients is limited. Therefore, both serum selenium concentration and 24 h urinary excretion of selenium were evaluated throughout the hospital course for 23 patients with partial and full skin thickness thermal burns. Serum selenium levels were depressed throughout the hospital course in the majority of patients, and only two patients' serum selenium levels had reached the normal range by discharge. Urinary selenium losses were essentially within normal range throughout the same period and thus were not responsible for the observed depression in serum selenium levels. A possible antagonistic relationship between selenium and silver is discussed.
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PMID:Serum and urinary selenium levels in thermal injury. 371 97

The mechanisms of toxicity and sensitization by the radiosensitizer misonidazole [1-(2-nitro-1-imidazolyl)-3-methoxy-2-propanol] are not well understood. We report here on the inhibition of total glutathione peroxidase (GSHPx), selenium-dependent glutathione peroxidase (selenium-GSHPx) and glutathione transferase (GSHTx) activities by misonidazole. Mouse liver cytosol GSHPx and selenium-GSHPx were inhibited in vitro with 0.5 mM misonidazole. On administration of the drug intraperitoneally (800 mg/kg) to mice, it was found that GSHPx, selenium-GSHPx, and GSHTx were inhibited in homogenate, cytosol, and microsomal fractions of mouse liver. GSHPx was depressed in all fractions up to 60-70% of control values, with maximum depression occurring in the cytosol and homogenate fractions in less than 2 hr. Recovery of activity was slower in the microsomes. In general, the pattern of depression of selenium-GSHPx was parallel to that of GSHPx except in microsomes, where GSHPx is minimal. Quantitatively, selenium-GSHPx was least affected. GSHTx was inhibited 70-80% of control values in cytosol and homogenate with recovery by 24 hr, whereas a second period of depression occurred at 24 hr in the microsomes. The inhibition of peroxide-metabolizing enzymes may lead to elevation of intracellular peroxide levels, contributing to the radiosensitizing effect and/or toxicity of misonidazole.
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PMID:Inhibition of glutathione peroxidase and glutathione transferase in mouse liver by misonidazole. 375 20

The effects of the xenobiotics, i.e. butylated hydroxytoluene, beta-naphthoflavone, isosafrole, pregnenolone-16 alpha-carbonitrile, trans-stilbene oxide, 3-methylcholanthrene, phenobarbital, 3,3',4,4'-tetrachlorobiphenyl, 2,2',4,4',5,5'-hexachlorobiphenyl, on rat liver cytosolic glutathione transferase and glutathione peroxidase activities have been investigated. Although the glutathione transferase isozymes (measured by the specific substrates ethacrynic acid and delta 5-androstene-3,17-dione) which have been shown to possess peroxidase activity were significantly increased, little or no increase in peroxidase activity (toward cumene hydroperoxide, tert-butyl hydroperoxide or hydrogen peroxide) was observed. Likewise during a 16-day time course following the administration of Aroclor 1254 or fireMaster BP-6 (each 500 mg/kg, i.p.), potent induction of glutathione transferase activities was seen without any significant increases in peroxidase activities. In fact during the second week of the time course, there were significant decreases in selenium-dependent glutathione peroxidase activity (toward hydrogen peroxide). The inverse regulation of these activities, i.e. the depression of selenium-dependent glutathione peroxidase activity following sustained induction of glutathione transferases, may have direct implications for the toxicity of the polyhalogenated aromatic hydrocarbons.
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PMID:Differential regulation of hepatic glutathione transferase and glutathione peroxidase activities in the rat. 405 12

Plasma cortisol levels were estimated by the competitive protein binding (CPB) method with radioactive selenium-75 in 32 male chronic alcoholics with depression. The degree of depression was rated by the Hamilton Depression Rating Scale (HDRS). Duration of drinking ranged from 5-25 years with an average daily amount of ethanol intake of 100-150 g (equivalent to half a bottle of spirits). Plasma cortisol levels were often raised in drinking chronic alcoholics and there was a strongly positive and statistically highly significant correlation between them and depression ratings (r = +0.56; P = 0.001). It is possible that the diurnal rhythm of cortisol secretion is disturbed or adreno-cortical activity is stimulated in these patients due to chronic ethanol ingestion. It is further suggested that brain serotonin deficiency known to occur in chronic alcoholics might lead to raised plasma cortisol levels in ethanol-induced depression.
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PMID:Relationship between plasma cortisol concentrations and depression in chronic alcoholic patients. 614 9

The treatment of rats with 10 mumoles/kg (s.c.) of mercuric chloride (Hg2+) caused time-dependent decreases in the activities of the enzymes of the glutathione (GSH) metabolism pathway in the kidney. Twenty-four hours after administration of Hg2+, the activities of gamma-glutamylcysteine synthetase and glutathione disulfide (GSSG)-reductase in the kidney were decreased by 50-60%, and the activities of the GSH catabolic enzymes, gamma-glutamyl transpeptidase and GSH-peroxidase, were decreased by 25-35%. In the liver, only the activity of GSSG-reductase was decreased at this time. The observed decreases in the enzyme activities were not accompanied by a depression in the cellular protein concentration. The same pattern of enzyme response was noted when rats were given 30 mumoles/kg Hg2+; however, the decreases in the specific activity of the enzymes were accompanied by great losses in the cellular protein concentrations in both the liver and the kidney (35-40%). This dose of Hg2+ also caused significant decreases in the concentration of GSH in both organs. In vitro, Hg2+ only inhibited the activity of GSSG-reductase. When rats were given sodium selenite (Na2SeO3; 5, 10 or 20 mumoles/kg, s.c.) 30 min after Hg2+ treatment (10 mumoles/kg), the Hg2+-related depressions in the activities of the enzymes of GSH metabolism in the liver and the kidney were blocked. Also, in rats treated with 30 mumoles/kg Hg2+, the administration of 10 mumoles/kg selenium significantly decreased the magnitude of depression in the concentration of GSH in the kidney.
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PMID:Inhibition of the enzymes of glutathione metabolism by mercuric chloride in the rat kidney: reversal by selenium. 621 90

Effect of sodium selenite on renal toxicity and antitumor activity of cis-diamminedichloroplatinum (Cisplatin; CDDP) repeatedly administered to mice inoculated with Ehrlich ascites tumor cells were examined. Simultaneous repeated administration of selenite with CDDP markedly improved the growth depression, the renal toxicity indicated by blood urea nitrogen value and the diarrhea caused by CDDP, and inhibited the growth of Ehrlich ascites tumor cells cooperatively with CDDP. This results suggest that selenium compounds are useful for prevention of the toxic side effects of CDDP.
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PMID:Effect of selenite on renal toxicity and antitumor activity of cis-diamminedichloroplatinum in mice inoculated with Ehrlich ascites tumor cell. 654 Mar 2

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

Comparative study of isolated retinas of frogs and turtles exposed to rhythmical photostimulation was conducted. It was shown that there are marked differences between the responses of isolated retinas of frogs and turtles to the rhythmical photostimulation. A considerable depression of the total amplitude of the rhythmical electroretinogram was observed under the conditions of induced lipid peroxidation. Introduction of a selenium compound to the superfusing medium increased to a certain extent both the single and rhythmical responses of isolated retinas of the animals.
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PMID:[Dynamics of changes in the electroretinogram of isolated frog and turtle retinas during rhythmic photic stimulation in conditions of induced lipid peroxidation]. 672 97

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


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