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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Undernutrition may exacerbate hyperoxia-induced lung injury, a finding that may be of significance in the early clinical management of the premature human infant. Addressing this specific problem, we found that 72 h of food restriction in guinea pig pups delivered 3 days preterm increased mortality rates among pups exposed to 95% oxygen (8/18) and yet had no effect on 21% oxygen (air)-exposed pups (0/10). Reduced tolerance of hyperoxic conditions was not, however, associated with increased lung injury, assessed as pulmonary microvascular leakage. Pulmonary antioxidant enzyme activities [Cu,Zn superoxide dismutase (SOD), Mn SOD, glutathione peroxidase, and catalase] were unaltered by starvation or hyperoxia. Lung glutathione concentration was slightly decreased after food restriction, whereas hyperoxic exposure did not change either lung or bronchoalveolar lavage fluid glutathione concentrations or lung antioxidant enzyme activities. Increased susceptibility to the lethal effects of oxygen in the starved preterm guinea pig pup could not be attributed to a deficiency of pulmonary antioxidant defenses.
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PMID:Effect of food restriction on hyperoxia-induced lung injury in preterm guinea pig. 141 61

Adult, term neonatal and 3 day preterm neonatal guinea pigs were fasted for 48 hr, and the glutathione concentrations of the liver and lung assessed. In adult animals, glutathione concentration decreased by 43% in the liver and 29% in the lung with respect to fed controls. The decrease in liver glutathione was associated with a 75% reduction in the hepatic activity of tau-glutamyltranspeptidase (tau GGT). Conversely, both liver and lung glutathione levels in preterm pups remained unchanged following 48 hr food restriction. Likewise, hepatic tau GGT, glutathione reductase (GRed) and glutathione peroxidase (GPx) activities were unchanged by fasting in preterm pups. Fasting increased pulmonary GPx activity by 27% in these pups. In fasted, term animals, substantial increases in both lung (65%) and liver (80%) glutathione concentrations were observed, with concomitant increases in GPx and GRed activities. Hepatic tau GGT activity was significantly reduced (57%) in term pups. These results may suggest that the neonatal guinea pig can maintain tissue glutathione status during periods of nutrient stress, through an increased capacity for recycling oxidized glutathione and a decrease in turnover of the tripeptide. Guinea pig neonates are therefore able to resist starvation-induced decreases in tissue glutathione levels seen in adult rodents. If this is a general neonatal response it may have important clinical implications in the treatment of preterm babies.
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PMID:Differing response of the glutathione system to fasting in neonatal and adult guinea pigs. 141 72

The effects of selenium (Se) deficiency on urinary ketone body excretion in starved rats were examined. Rats were fed a basal diet which was Se-deficient (Se content: 0.011 micrograms/g) or a Se-adequate diet (the basal diet supplemented with 0.1 micrograms Se/g as sodium selenite). On the 11th and 22nd week of the feeding period, Se-deficient status in rats fed the basal diet was verified by the observation that the Se content and glutathione peroxidase activity in their plasma, erythrocytes, and livers were markedly lowered. On the 4th, 6th, 11th, 15th, and 22nd week, the rats were starved for 48 h and the urinary excretion of ketone bodies (acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA)), urea, and creatinine were examined. The urinary excretion of AcAc and 3-OHBA during the second 24 h of the 48-h starvation period were markedly higher in the Se-deficient rats than in the Se-adequate rats for all weeks examined, while the urine volume and the excretion of urea and creatinine were similar in the Se-deficient and Se-adequate rats, irrespective of the feeding period and the number of hours of starvation. On the 22nd week, the plasma ketone body levels were also determined and significantly higher plasma 3-OHBA levels were observed in the Se-deficient rats than in the Se-adequate rats 72 h after starvation began. These results indicate that Se deficiency causes an increase of urinary ketone body excretion in starved rats and that the increase is ketone-specific with no changes in major urinary profiles.
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PMID:Increase of urinary ketone body excretion in selenium-deficient rats is a ketone-specific change. 176 47

Distribution of glutathione reductase (GR) and selenium-dependent glutathione peroxidase (GP) activity and the content of selenium in the cytosolic fraction of the brain stem, hypothalamus and different cortical areas of the rat cerebrum in norm and under starvation was investigated. It was shown that GR activity in all investigated structures was approximately identical, but GP activity in various cortical areas was 1.5-2.0 times higher, than that in the mesencephalon and myeloencepalon. During 2-3 days of starvation GR activity changed insignificantly, whereas GP activity varied within wide limits. Under prolonged starvation a significant decrease in the content of selenium and GP activity was observed. The correlation of these changes was more expressed in the hypothalamus. It was assumed that glutathione and enzymes of its metabolism were involved in the regulatory system of redox processes in the nervous tissues in the primary period of starvation.
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PMID:[Glutathione defense system in various brain structures during starvation]. 178 76

Starvation for 24 h causes a striking fall in glutathione content from 3.19 +/- 0.27 to 1.88 +/- 0.14 (X +/- SEM) mumol/g tissue and of GGT activity from 31.75 +/- 4.17 to 19.49 +/- 3.13 (X +/- SEM) nmol/min/mg protein in the homogenate from whole mucosa of the upper small intestinal segments. This was associated with a significant increase in GSH-Px activity and the content of lipid peroxides (measured by the thiobarbituric assay). On semi-synthetic iron-supplemented diet the activities of GSH-T and GGT were significantly decreased as compared with crude diet. On semisynthetic iron-depleted diet GSH-T and GGT activities were further depressed, but this was accompanied with an additional depression of GSH, glutathione reductase (GSSG-R), and glutathione peroxidase (GSH-Px) activities and lipid peroxide concentrations. Food deprivation significantly lowers the mucosal GSH-content and could lead to a destabilization of this system presumably by increased oxidative stress. As compared to normal "crude" diet, semisynthetic diets and oral iron depletion have been shown to cause a depression of the intestinal GSH system. As a consequence of these effects, the resistance of the small intestinal mucosa toward exogeneous dietary toxins might be reduced.
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PMID:Glutathione and its related enzymes in the small intestinal mucosa of rats: effects of starvation and diet. 256 68

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 the rat remnant kidney hydrogen peroxide (H2O2) production is increased when compared to the normal kidney. The activities of the peroxisomal H2O2-producing oxidases, D-amino acid oxidase and acyl-coenzyme A oxidase, and of the extraperoxisomal superoxide dismutase are decreased in renal homogenate. The peroxisomal L-alpha-hydroxyacid oxidase and L-lactate oxidase as well as the peroxisomal H2O2 scavenger catalase preserve their activity. The activity of the cytosolic scavenging system, glutathione peroxidase, is decreased by 40%. A starvation period of 48 h does not produce a measurable increase in H2O2 production in the normal nor in the remnant kidney. On visual inspection, peroxisomal morphology and distribution in the renal tubules are similar in the normal and remnant kidney tissue.
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PMID:In vivo hydrogen peroxide production in rat remnant kidney. 752 73

Manganese superoxide dismutase (MnSOD) levels were monitored as a function of time in culture to determine whether these levels were altered at logarithmic growth versus when the cells exhibited density limitation of growth. For comparison, activities of the antioxidant enzymes copper, zinc superoxide dismutase (CuZnSOD), catalase, and glutathione peroxidase were also evaluated. Four cell lines were studied, two of which exhibited density limitation of growth and two of which did not. Each cell line showed a unique antioxidant enzyme profile. The two cell lines that showed density limitation of growth also demonstrated induction of MnSOD at the time when the cells stopped proliferating in culture, whereas the other two cell lines did not show induction of MnSOD. There was no strict correlation between density limitation of growth and activities of the other antioxidant enzymes. To determine whether SOD varied with various phases of the cell cycle, NIH/3T3 cells were synchronized using serum starvation, and then SOD activities were measured during quiescence (G0) and the phase of DNA synthesis (S-phase). MnSOD was decreased during S-phase compared with G0, whereas CuZnSOD was increased during S-phase compared with G0, demonstrating alteration of SOD activities with varying phases of the cell cycle. This study suggests the possibility that increased MnSOD may correlate with decreased cell proliferation and suggests significant alterations in SOD activities during the cell cycle.
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PMID:Antioxidant enzyme levels as a function of growth state in cell culture. 763 59

The effects of three-day fasting and one-day refeeding on some blood metabolites and parameters of lipid peroxidation were studied in eight non-pregnant merino ewes. Fasting produced an immediate decrease in blood glucose accompanied by an increase of free fatty acid, total lipid, total cholesterol and urea in the plasma. Starvation increased the concentration of thiobarbituric acid-reactive substances (malondialdehyde), with a slower but more sustained increase in the plasma than in the red blood cell haemolysate. Changes in glutathione peroxidase activity were the reverse of those in malondialdehyde concentration. Catalase activity was not measurable in plasma but was consistently increased in the haemolysate on fasting. Superoxide dismutase activity in the whole blood haemolysate significantly increased only on the first day of food deprivation. The vitamin E content of plasma showed no significant changes. The results indicate that energy deficiency, a well-known phenomenon in ruminants, affects not only the metabolic parameters of the blood but its lipid peroxidative status as well.
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PMID:Effect of fasting on blood lipid peroxidation parameters of sheep. 839 31

Considerable evidence suggests that oxidative stress plays an important role in tissue damage associated with hypoglycemia and other metabolic disorders. The altered brain neurotransmitters metabolism, cerebral electrolyte contents, and impaired blood-brain barrier function may contribute to CNS dysfunction in hypoglycemia. The present study elucidates the effect of starvation and insulin-induced hypoglycemia on the free radical scavanger system--reduced glutathione (GSH) content, glutathione S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GR), gamma-glutamyl transpeptidase (gamma-GTP), gamma-glutamyl cystein synthetase (gamma-GCS), catalase and superoxide dismutase (SOD), and mitochondrial electron transport chain (ETC) complexes I-IV from three different regions of rat brain, namely cerebral hemispheres (CH), cerebellum (CB), and brainstem (BS). Peripheral organs, such as liver and kidney, were also studied. Significant changes in these enzymic activities were observed. The analysis of such alterations is important in ultimately determining the basis of neuronal dysfunction during metabolic stress conditions, such as hypoglycemia, and also defining the nature of these changes may help to develop therapeutic means to cure metabolically stressed tissues.
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PMID:Effect of starvation and insulin-induced hypoglycemia on oxidative stress scavenger system and electron transport chain complexes from rat brain, liver, and kidney. 1032 15


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