Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in endogenous free radical-scavenging defense mechanisms of rat tissues after body weight loss (induced by starvation for 72 h) associated with hypoinsulinemia were investigated. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and glutathione (GSSG) reductase as well as levels of reduced glutathione (GSH) were examined in several tissues and in erythrocytes. A complex pattern of changes was observed. CAT activities were increased in the heart and pancreas and decreased in the liver. SOD levels were decreased in the heart and increased in the kidney and pancreas. GSH-PX activities were increased only in the kidney, and levels of GSH were decreased only in the liver of starved animals. Erythrocytes from starved animals showed no alterations in the levels of major free radical-scavenging enzymes. However, GSSG reductase levels were lower in erythrocytes from starved animals, and this was associated with an increased susceptibility to H2O2-induced GSH depletion. Paradoxically, H2O2-induced malondialdehyde (MDA) production in erythrocytes from starved animals was lower than that in control erythrocytes. Our results suggest that, in studies of experimental diabetes, attention must be given to the influence of body weight loss per se on the biochemical alterations associated with this disease.
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PMID:Starvation-related alterations in free radical tissue defense mechanisms in rats. 380 31

In most types of experimentally induced cataracts, glutathione (GSH) content decreases considerably before the onset of opacity. GSH may provide a protective function for protein SH groups by scavenging oxidative products that may impair lens metabolism. To avoid impairment of lens metabolism by decreased levels of GSH it may be possible in vitro: (1) to stimulate GSH synthesis by enrichment of the incubation medium with the amino acids necessary for GSH synthesis or (2) to enrich the incubation medium with the tripeptide itself so that it can be taken up by the lens. Both approaches were investigated with bovine lenses. Lenses were incubated in pairs in a salt solution without carbohydrates, so as to deplete lens of GSH. Following starvation, one lens of each pair was incubated for recovery in TCM 199 enriched with MgSO4 and the three amino acids of GSH; the other lens was put into a freshly prepared salt solution. After 6 h, lenses from the recovery solution contained more GSH than the other lenses. Addition of fructose-1,6-diphosphate to the medium enhanced this effect. When, after starvation, lenses were incubated in the presence of different amounts of GSH, GSH lens content rose, with the highest in those lenses incubated in a medium with a final molarity of 4 X 10(-3) M GSH. Therefore, incubation of lenses depleted of GSH in medium with either the amino acids of GSH or GSH itself appear to facilitate recovery of GSH content.
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PMID:Is it possible to maintain a normal glutathione level in lenses in vitro? 397 34

Mouse liver glutathione content showed a diurnal variation with a maximum GSH + 2 GSSG content at 6 to 10 a.m. of 62 +/- 8 nmole per mg protein and a minimum of 42 +/- 7 at 6 p.m. Starvation for more than 24 hr decreased the hepatic glutathione content to 22 +/- 3 nmole/mg protein and abolished the diurnal rhythm. Artificial reversal of the feeding habit of the animals reversed the diurnal rhythm. Kidney, spleen and lung glutathione contents showed no such rhythm. The organ glutathione content decreased by 50% or more upon starvation. The increase of the liver glutathione content by injection of either free or liposomally entrapped GSH to starved animals was not dependent on the time of administration. The physiological maximum level could not be exceeded by this treatment. It was not possible to influence the glutathione content of kidney, lung or intestine by glutathione injections in either form. Intravenous injections of equimolar doses of 2,3-dimercaptopropanol, 2-mercaptoethanesulfonic acid, N-2-mercaptopropionylglycine, D-penicillamine, or cysteamine did not lead to any significant change in liver, kidney, spleen or lung glutathione contents 2 hr after administration. Intravenously given N-acetylcysteine, methionine, GSH or GSSG restored liver glutathione levels of starved animals to the contents observed in the fed state. The diurnal hepatic variation of GSH caused by the food intake habit of the animals may limit the capacity of the intracellular detoxication system.
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PMID:Diurnal fluctuation and pharmacological alteration of mouse organ glutathione content. 403 39

The herbicide paraquat was used to investigate the effects of oxidative stress on the spherulation of Physarum polycephalum microplasmodia. The responses of a white non-differentiating strain of Physarum were compared with those of a common yellow strain that readily spherulates in salts-only starvation medium. The addition of paraquat to the salts medium increased the specific activity of superoxide dismutase in both strains; it also induced an increase in the intracellular inorganic peroxide concentration in both strains. Glutathione concentration was higher in the paraquat-treated yellow strain than in the controls. Paraquat had no effect on glutathione concentration in white microplasmodia. Paraquat accelerated spherulation in yellow microplasmodia. The white microplasmodia responded to the herbicide by cleaving into structures similar to immature spherules; however, these structures were not viable. The results of this study support the hypothesis that free radicals are involved in cell state transitions.
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PMID:Effects of the free radical generator paraquat on differentiation, superoxide dismutase, glutathione and inorganic peroxides in microplasmodia of Physarum polycephalum. 406 5

Plasma amino acid concentrations have been investigated in 12 female patients with rheumatoid arthritis (RA), who were hospitalized for two 14-day periods, one of which included 7 days of total fasting, whereas the other served as control period with normal food intake. All medical treatment was stopped on admission to the hospital. Plasma amino acid levels were repeatedly determined during both periods. Another group, consisting of 8 healthy volunteers, also underwent total fasting, for 6 days. The response to food deprivation with regard to plasma amino acid levels was compared with that in the RA patients. The results obtained from the control period were compared with those derived from age and sex matched healthy controls. RA disease was not characterized by a typical amino acid pattern. Major increases were seen in the concentrations of taurine, aspartate, glutamate, glycine, 1-methyl histidine, isoleucine and arginine. Rather smaller yet significant elevations could be observed in the levels of cystein, threonine, serine, citrulline, methionine and leucine. The only amino acid to show a lowered concentration was alpha-aminobutyrate. Most of the alterations induced by fasting were similar to those in healthy volunteers. An exception was the levels of taurine, which evidenced in RA patients a further increase during starvation, not observed in healthy volunteers, and valine which exhibited, a smaller increment than that apparent in healthy controls. The increase in sulphur-containing amino acids might be interpreted as a sign of an enhanced glutathione (GSH) catabolism, whereas the differing metabolic behaviour of branched chain amino acids (BCAA) suggests a specific reaction of valine in RA disease, similar to that in other catabolic diseases.
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PMID:Plasma amino acids in rheumatoid arthritis. 408 62

1. Starvation for 3 days produces a decrease in methaemoglobin-reductase and glutathione-reductase activities, but it does not alter the glucose 6-phosphate-dehydrogenase activity of the rat erythrocyte. 2. The feeding of a protein-free diet for 11 days causes greater changes in the first two enzymes and also a diminution of the third. Under this experimental condition slight decreases in protein and haemoglobin contents were noted. 3. The experimental animals did not show methaemoglobinaemia, probably because the activity of methaemoglobin diaphorase is preserved. 4. The GSH content was not affected but the stability of the tripeptide in the presence of an oxidizing agent was diminished.
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PMID:Studies on the oxidation-reduction systems of the erythrocyte. 437 99

The hepatic acid-soluble thiol content of striped mullet (Mugil cephalus) exposed to cadmium (10 mg/liter seawater), mercury (200 micrograms/liter), fluorene (100 micrograms/liter), dibenzofuran (750 micrograms/liter), or a 20% water-soluble fraction of a No. 2 fuel oil, and of winter flounder (Pseudopleuronectes americanus) exposed to pentachlorophenol (200 micrograms/liter) for up to 3 weeks was determined. Exposure to these chemicals caused an elevation of hepatic acid-soluble thiol content over control values. Similarly, the acid-soluble thiol content was 1.75 times control values 24 hr after injection with acetaminophen (40 mg/100 g body wt, ip). In contrast, hepatic acid-soluble thiol concentrations did not fluctuate after feeding or during short-term starvation, or after acute or chronic physical trauma. Thus, the increase in hepatic acid-soluble thiols observed in mullet appears to be a specific response to chemical insult. The effect of chemical exposure on specific thiols can vary with the compound under investigation. Glutathione accounted for most of the acid-soluble thiol increase observed in mullet exposed to oil, whereas other acid-soluble thiols were also elevated after exposure to cadmium. Injection of [14C]glycine into cadmium- and oil-treated mullet showed that hepatic uptake of this amino acid substrate and its incorporation into hepatic glutathione increased after chemical exposure. The proportion of the total [14C]glycine in the liver incorporated into glutathione was unchanged after oil exposure, but was significantly increased in cadmium-exposed fish. These results suggest that chemicals may elevate glutathione content by enhancing the hepatic uptake of amino acid substrates and also the activity of biosynthetic enzymes.
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PMID:Effects of metals and organic compounds on hepatic glutathione, cysteine, and acid-soluble thiol levels in mullet (Mugil cephalus L.). 648 87

NMRI Albino mice, in which the hepatic glutathione (GSH) content was decreased by nearly 50% by either the administration of a pure glucose diet or by starvation, were intoxicated with aryl halides, bromobenzene, and iodobenzene (13 and 9 mmol/kg body weight, respectively, p.o.). After both intoxications, the hepatic glutathione content decreased rapidly to very low values, and liver necrosis, as assessed by serum transaminase levels, occurred in about 45 or 60% of the animals (in the case of bromobenzene or iodobenzene, respectively) after a lag phase of 9 or 6 hr. In both instances liver necrosis was evident only when the hepatic GSH depletion reached a threshold value (3.5-2.5 nmols/mg protein). The same threshold value was evident for the occurrence of lipid peroxidation (measured as both carbonyl functions and conjugated dienes in liver phospholipids). The possibility that the depletion in hepatic GSH level is capable of inducing lipid peroxidation and necrosis could be supported by the fact that similar results were obtained after the administration of inethylmaleate (12 mmol/kg, p.o.), a drug which is expected to conjugate directly with GSH without previous metabolism. The covalent binding of reactive metabolites to cellular macromolecules was determined in the case of bromobenzene poisoning. A dissociation between liver necrosis and covalent binding was observed in experiments in which Trolox C, a lower homolog of vitamin E, was administered (270 mumol/kg) 9 and 13 hr after bromobenzene poisoning. The treatment with Trolox C, in fact, almost completely prevented both liver necrosis and lipid peroxidation, while the extent of the covalent binding of bromobenzene metabolites to liver proteins was not altered.
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PMID:Glutathione depletion, lipid peroxidation, and liver necrosis following bromobenzene and iodobenzene intoxication. 651 83

The mechanisms underlying iodobenzene hepatotoxicity were investigated in Albino mice in which the hepatic glutathione (GSH) content had been decreased by nearly 50% by starvation for 16 h before poisoning. After iodobenzene administration (9 mmol/Kg, p.o.) the hepatic GSH content decreased progressively and liver necrosis, as measured by the plasma transaminase (GPT, GOT) levels, occurred in many animals at 12 and 16 h. A clear cut necrosis was evident only when the hepatic GSH depletion reached a threshold value (3.5-2.5 nmol/mg protein). The same threshold value was evident for the occurrence of lipid peroxidation (measured as both carbonyl functions and conjugated dienes in liver phospholipids). The highly significant correlation found between lipid peroxidation and liver necrosis supports the possibility of a cause-effect relationship between the two phenomena.
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PMID:[Depletion of liver glutathione induced by iodobenzene poisoning and its relation to lipid peroxidation and necrosis]. 666 14

Glutathione levels were determined in mosquitoes of all ages of the life span. Specific analyses for reduced (GSH) and oxidized (GSSG) glutathione were used and validated to ensure minimal autoxidation of GSH and conversion of these forms. Indeed GSH accounted for greater than 97% of the total glutathione (GSH + GSSG) content in all samples. Marked changes occurred during the life span, and the highest levels of GSH and total glutathione were found during larval growth and metamorphosis (P less than 0.001). Thereafter the levels decreased in the early adult, plateaued in the mature, and decreased 46% in the old and very old mosquito (P less than 0.001). This aging-specific decrease was a general phenomenon, for it occurred in all body regions of both sexes. Starvation up to 3 days did not affect the GSH levels. The importance of these changes in glutathione is its relationship to the reducing and biosynthetic capacities of different life span stages. Of special interest is the senescence decrease which can lead to lower biosynthetic activity and also impaired detoxification capacity.
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PMID:Glutathione levels during the mosquito life span with emphasis on senescence. 672 37


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