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)

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 effects of chronic alcohol feeding on biliary glutathione excretion were studied in rats pair fed diets containing either ethanol (36% of total energy) or isocaloric carbohydrate for 4-6 weeks. An exteriorized biliary-duodenal fistula was established and total glutathione (GSH) and oxidized glutathione (GSSG) were measured. A significant decrease was observed in rats fed alcohol chronically compared to their pair fed controls in the biliary excretion of GSH (55.7 +/- 37.0 vs 243.1 +/- 29.0 micrograms/ml bile, p less than 0.025) as well as biliary GSSG (12.5 +/- 5.0 vs 49.9 +/- 8.0 micrograms/ml bile, p less than 0.05) and in bile flow (23.1 +/- 1.6 vs 29.2 +/- 1.3 micrograms/min, p less than 0.05). An acute dose of ethanol tended to exaggerate the decrease on biliary GSH and GSSG in the two groups of animals. The depression in biliary GSH could not be attributed to decreased GSH synthesis since S35-L-methionine incorporation into hepatic and biliary GSH was unchanged or even increased after chronic ethanol feeding.
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PMID:Depression of biliary glutathione excretion by chronic ethanol feeding in the rat. 670 Mar 69

Single oral dosages of the synthetic narcotic analgesic, L-alpha-acetylmethadol (LAAM) increased serum glutamic-pyruvic transaminase (SGPT) levels throughout a two-day observation period and produced a persistent depletion of hepatic and renal glutathione (GSH) levels. These LAAM-induced changes demonstrated dose- and time-dependence within that dosage range producing mortality. Histological evaluation of livers from LAAM-treated mice revealed cytoplasmic and nuclear changes in centrilobular hepatocytes. Interestingly, neither the LAAM-induced histopathological changes nor the depression of hepatic GSH were altered by the induction of hepatic metabolism following pretreatment with either phenobarbital or 3-methylcholanthrene; however, the induction of hepatic drug metabolism did abate the four-day mortality and SGPT elevations.
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PMID:L-alpha-acetylmethadol-induced tissue alterations in mice. 672 48

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

Lipid peroxidation has been incriminated in some types of drug-induced liver injury, but it is unclear whether it contributes to or is present in alcoholic liver injury. In order to study this question, hepatic lipid peroxidation (measured as formation of diene conjugates) and hepatic GSH were assessed in baboons and rats after short- and long-term ethanol administration. Compared to controls, baboons fed alcohol for 1 to 4 years (chronic administration) had increased hepatic diene conjugates (16.9 +/- 4.8 OD/gm of liver) and depressed GSH (3.8 +/- 0.6 VS. 6.3 +/- 0.8 mumol/gm of liver; p less than 0.01) after an overnight withdrawal from ethanol. Administration of 1.6 gm/kg ethanol over 6 hr (acute administration) increased diene conjugates (17.6 +/- 4.3) and decreased GSH (3.2 +/- 0.5; p less than 0.01) in control animals and had an even greater effect in animals chronically fed alcohol (diene conjugates 48.5 +/- 9.2; GSH 1.8 +/- 0.3; p less than 0.001). In six rats fed alcohol for 5 to 6 weeks (chronic administration), an increase in diene conjugates was detected in microsomes (0.343 +/- 0.210 OD/mg of lipid) and mitochondria (0.143 +/- 0.061), accompanied by decrease in arachidonic acid and C22 polyenes, after acute ethanol administration (3 gm/kg p.o.) but no significant change in GSH. Simultaneous administration of methionine attenuated diene conjugate formation (0.107 +/- 0.058 and 0.035 +/- 0.020 OD/mg of lipid, respectively) and fatty acid changes. Thus chronic alcohol feeding potentiates lipid peroxidation produced by an acute dose of ethanol; these changes are not dependent on GSH depression but may be potentiated by it.
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PMID:Ethanol-induced lipid peroxidation: potentiation by long-term alcohol feeding and attenuation by methionine. 726 37

Glutathione (GSH) regeneration was studied in rabbit erythrocytes which were loaded with calcium using ionophore A23187. Calcium-loading induced by A23187 and various concentrations of CaCl2 caused a dose-dependent depression in red cell GSH regeneration. The lowered GSH regeneration was mainly due to reduction of ATP level. In an experiment using haemolysate, the effect of calcium per se was negligible, while magnesium strongly affected GSH regeneration by controlling the rate of hexokinase reaction. These results indicate a possibility that cation perturbation, metabolic decay and oxidative damage are all interrelated in the erythrocyte aging process.
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PMID:Glutathione regeneration in calcium-loaded erythrocytes: a possible relationship among calcium accumulation, ATP decrement and oxidative damage. 755 47

Oxidant stress alters protein structure and function, possibly through the modification of the redox status of regulatory protein sulfhydryl groups. We used the sulfhydryl-blocking reagent p-chloromercuriphenylsulfonic acid (pCMPSA), applied selectively and independently to either the intracellular or extracellular environment, to study the relationship between blocking protein sulfhydryl groups and Na(+)-K+ pump current (i.p.). In guinea pig ventricular myocytes voltage clamped at -30 mV, extracellular pCMPSA (50, 100, and 400 microM) caused a concentration-dependent reduction in holding current. The selective intracellular administration of pCMPSA (100 microM) induced a similar inhibition of i.p., albeit over a longer time course. The inhibition of ip resulting from either the intracellular or extracellular application of pCMPSA (100 microM) was reversed, in part, by the extracellular application of dithiothreitol (3 mM). An intracellular oxidant stress was also imposed by using diethyl maleate to deplete the intracellular nonprotein sulfhydryl content [represented by reduced glutathione (GSH)]. In myocytes isolated from diethyl maleate-treated guinea pigs *860 mg/kg i.p., 30 min before study), intracellular GSH was depleted by 93% and i.p. was depressed by 38% at all membrane potentials tested. We propose that Na(+)-K+ pump function may be related to protein and nonprotein sulfhydryl status. Protein sulfhydryl oxidation and glutathione depletion may account, in part, for a depression in Na(+)-K+ pump activity during reperfusion-induced oxidant stress.
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PMID:Modulation of cardiac Na(+)-K+ pump current: role of protein and nonprotein sulfhydryl redox status. 763 60

The primary defence mechanism of myocytes against peroxides and peroxide-derived peroxyl and alkoxyl radicals is the glutathione redox cycle. The purpose of the present study was to increase the turnover rate of this cycle by stimulating the glutathione peroxidase catalysed reaction (2GSH-->GSSG), the glutathione reductase catalysed reaction (GSSG-->2GSH), or both. Neonatal rat heart cell cultures were subjected to a standardized protocol of oxidative stress using 80 mumol.l-1 cumene hydroperoxide (CHPO) for 0-90 min. The consequences of this protocol were described in terms of cellular concentrations of GSH, GSSG, NADPH and ATP, formation of malondialdehyde (MDA), release of GSSG and of ATP catabolites, depression of contraction frequency, cellular calcium overload, and enzyme release. Trolox-C, an analogue of vitamin E, accelerated the glutathione peroxidase reaction leading to lowering of GSH concentration and the GSH/GSSG ratio, less MDA formation, diminished negative chronotropy, delayed calcium overload, and less enzyme release. Glucose was used to accelerate the glutathione reductase reaction by supplying NADPH, leading to higher GSH concentration and a higher GSH/GSSG ratio, less MDA formation, diminished negative chronotropy, unchanged development of calcium overload, and less enzyme release. As a full turn of the glutathione redox cycle involves both the peroxidase and the reductase reactions, the combination of Trolox-C and glucose was superior to either of the two alone: 90 min following addition of CHPO together with Trolox-C and glucose, the GSH concentration and the GSH/GSSG ratio were almost normal, MDA formation was extremely low, calcium overload was markedly delayed, and enzyme release hardly occurred at all. Cells remained beating in the observation period of 30 min. We conclude that the capacity of the glutathione redox cycle to withstand oxidative stress can be increased by stimulation of either the peroxidase reaction or the reductase reaction, and that optimal redox cycling is achieved by stimulation of both reactions.
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PMID:Protection of myocytes against free radical-induced damage by accelerated turnover of the glutathione redox cycle. 767 3

When male guinea pigs were given a single dose of Cd (2.0 mg Cd2+/kg, ip) 72 hr prior to sacrifice, the hepatic reduced glutathione (GSH) level did not change although glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene (DCNB), ethacrynic acid (EAA), and 1,2-epoxy-3-(p-nitrophenoxy) propane (ENPP) increased significantly as compared to controls. Cd did not change the renal GSH level and GST activities toward CDNB and EAA. However, significant increase was observed in the GST activity for DCNB whereas GST activity for ENPP was significantly inhibited by Cd. When the animals were given a single dose of Ni (14.8 mg Ni2+/kg, sc) 16 hr prior to sacrifice, significant increases were observed in hepatic GSH level and GST activities toward CDNB, DCNB, EAA and ENPP. Ni, however, depressed the renal GSH level and GST activities toward CDNB, DCNB and ENPP significantly. The renal GST activity toward EAA remained unaltered. For the combined treatment, guinea pigs received the single dose of Ni 56 hr after the single dose of Cd and then they were killed 16 hr later. In these animals, no significant alteration was observed in the hepatic GSH level. The augmentation of elevation was observed in hepatic GST activities toward CDNB and DCNB. Combined metal treatment did not potentiate the elevation of hepatic GST activities toward EAA and ENPP to any greater degree. The depression of renal GSH level was significantly ameliorated by the combined treatment. Combination treatment potentiated the depression of renal GST activity for ENPP but not for CDNB.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential combined effect of cadmium and nickel on hepatic and renal glutathione S-transferases of the guinea pig. 769 89

Potential scavenging properties of cephalosporins (i.e. cefamandole, cefotaxime and ceftriaxone) towards hypochlorous acid (HOCl) as well as the antibacterial activity of control and HOCl-reacted antibiotics were investigated. We found that these drugs, at therapeutically relevant concentrations, are indeed scavengers of HOCl, with ceftriaxone showing the highest anti-HOCl capacity. However, the efficiency of cephalosporins in protecting biological molecules is also related to the chemical identity of such molecules. Indeed, the polyenoic compound beta-carotene is much better protected that the thiol compound GSH against HOCl attack. Moreover, the drugs do not appear to form chloramine derivatives as a result of their reaction with HOCl, and they inhibit taurine-chloramine formation. After HOCl challenge, the antibacterial activity of cefamandole, cefotaxime and ceftriaxone (tested against the standard strain Escherichia coli ATCC 25922) is approx. 8-, 5- and 4-fold lower, respectively, than that of the HOCl-unreacted antibiotics. The depression of the antibacterial activity of cephalosporins appears inversely related to their HOCl scavenging capacity, suggesting that the drug antioxidant groups may protect the beta-lactam ring against HOCl attack. In conclusion, physiological biomolecules are protected by cephalosporins against HOCl-driven oxidative injury with varying efficiency, this antioxidant defence being a consequence of a direct drug scavenging capacity towards HOCl. The interaction of cephalosporins with HOCl, however, results in a depression of their antibacterial activity.
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PMID:Cephalosporins are scavengers of hypochlorous acid. 776 5


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