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Query: UMLS:C0042875 (vitamin E deficiency)
 916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Age-related alterations in both antioxidant capacity and lipid peroxidation in the cerebrum, lung and liver homogenates of normal and vitamin E-deficient rats were investigated. The antioxidant capacity, which includes superoxide dismutase, catalase and glutathione peroxidase activities and vitamin E (alpha-tocopherol) concentration, was relatively stable throughout the lifespan. It was observed, however, that catalase and glutathione peroxidase activities in livers of old rats decreased and that vitamin E concentration in lung and liver increased with age. In vitamin E-deficient animals, catalase activity in liver increased and glutathione peroxidase activity in liver and lung decreased. Lipid peroxidation was monitored by use of three different indices, i.e. the thiobarbituric acid (TBA) value, oxygen absorption and conjugated-diene formation. In the absence of any initiator, neither oxygen absorption into tissue homogenates nor conjugated-diene formation in lipid extracts from the homogenates occurred. The TBA value of each cerebrum homogenate incubated under air or an oxygen atmosphere was larger than that of the corresponding unincubated cerebrum homogenate. From comparison between the TBA value and oxygen absorption, this increase in the TBA value was suggested to be due to some reactions other than lipid peroxidation. Although tissue homogenates examined contained TBA-reacting materials, no lipid peroxidation seems to arise during incubation of them. No age-related alterations in the TBA value and oxygen absorption in rat tissue homogenates were observed. Vitamin E deficiency had no effect on the TBA values of cerebrum and lung homogenates, while it seemed to increase the TBA values of liver homogenates. Vitamin E deficiency had no effect on oxygen absorption in these tissue homogenates. The induction period of initiator-induced conjugated-diene formation in lipid extracts from liver and lung homogenates from normal and vitamin E-deficient rats tended to be extended with age. Vitamin E deficiency decreased the induction period of initiator-induced conjugated-diene formation. As a result, the length of the induction period was found to be proportional to vitamin E concentration in lipid extracts. The overall antioxidant capacity of rat tissues appears to be maintained without large variation during ageing. Decreases in the capacity of some antioxidant factors may be compensated by increases in the capacity of other factors.
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PMID:Age-related alterations in antioxidant capacity and lipid peroxidation in brain, liver, and lung homogenates of normal and vitamin E-deficient rats. 140 85

To determine whether vitamin E protects against thyroxine-induced oxidative stress in heart and soleus (slow oxidative) muscles, lipid peroxide (thiobarbituric acid-reactive substances) and antioxidant enzymes were measured in those tissues of hyperthyroid rats supplemented with vitamin E. The rats were rendered hyperthyroid by the administration of L-thyroxine in their drinking water. In experiment (EXPT) I, 30 mg/kg/dose of alpha-tocopheryl acetate was administered to the vitamin E-treated group. In EXPT II, the rats were fed a diet containing either less than 1 IU/kg (deficient diet), 20 IU/kg (control E diet), or 500 IU/kg (high E diet) of vitamin E and hyperthyroidism was induced. In EXPT I, hyperthyroidism induced an increase in oxidative enzymes, mitochondrial superoxide dismutase and lipid peroxide level, and a decrease in cytosolic superoxide dismutase, glutathione peroxidase and catalase in both tissues. Vitamin E treatment inhibited the increase in lipid peroxide level totally in the heart and partially in the soleus, with minimal changes in the other biochemical indices studied. In EXPT II, the lipid peroxide level was markedly increased in both tissues of the vitamin E-deficient group, and decreased in those of the group fed high E diet. There were some adaptive changes in the levels of cytosolic superoxide dismutase, glutathione peroxidase, and catalase in response to vitamin E deficiency, whereas neither oxidative enzymes nor mitochondrial superoxide dismutase were altered. These results suggest that vitamin E protects against lipid peroxidation in hyperthyroid heart and skeletal muscle independently of the changes in oxidative enzymes and antioxidant enzymes.
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PMID:Vitamin E protects against thyroxine-induced acceleration of lipid peroxidation in cardiac and skeletal muscles in rats. 263 76

The effects of feeding vitamin E-deficient diets to rats for one year were investigated to analyse the relationship of the vitamin with other antioxidants and some antioxidative enzymes. Long-term vitamin E deficiency lowered the levels of antioxidants like vitamin E, ascorbic acid and glutathione (GSH) in all tissues analysed and thus increasing the extent of tissue peroxidisability. Vitamin E deficiency had also influenced the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase, the enzymes that are involved in detoxification mechanisms of products arising from free radical metabolism.
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PMID:Physiological antioxidants and antioxidative enzymes in vitamin E-deficient rats. 318 81

There is increasing evidence that islet beta cells may be susceptible to redox insult, and that this susceptibility may contribute to the pathogenesis of experimental models of diabetes mellitus. We investigated the effect of vitamin E deficiency, selenium deficiency, and combined deficiency on islet function and free radical scavenging systems. The tissue levels of glutathione peroxidase, catalase, and immunoreactive superoxide dismutases were measured in four groups of rats (i.e., controls and those with vitamin E, selenium, and combined deficiency). Glucose tolerance tests were performed for each animal before sacrifice. Superoxide dismutase concentrations in liver, heart, and skeletal muscle were within 20% of the control levels in all groups. However, the manganosuperoxide dismutase concentrations in islets were significantly lower than control levels in response to vitamin E, selenium, and combined deficiency. Combined deficiency appeared to have an additive effect. In contrast, cuprozinc superoxide dismutase concentration in islets was higher in the deficient groups than in controls. Insulin secretory reserve was decreased in each of the three deficient groups. This decrease was reflected as glucose intolerance only in the group with combined deficiency. Glutathione peroxidase activity was markedly decreased in selenium-deficient animals in all tissues studied. Catalase activity did not change significantly among groups in any tissue studied. Islets had the lowest glutathione peroxidase and cuprozinc and total superoxide dismutase levels among tissues studied.
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PMID:Effect of vitamin E deficiency and selenium deficiency on insulin secretory reserve and free radical scavenging systems in islets: decrease of islet manganosuperoxide dismutase. 351 3

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.
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PMID:Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence. 359 58

Effects of vitamin E deficiency and its restoration on biochemical characteristics of hepatic peroxisomes were studied. Rats were maintained on the vitamin E-deficient diet for 25 weeks and then on a diet supplemented with vitamin E for 5 weeks. Blood hemolysis by hydrogen peroxide and lipid peroxidation in the liver increased markedly in vitamin E-deficient rats. The former returned to the control level after the resupplying of vitamin E, but the latter did not. Of liver peroxisomal enzymes, the activities of catalase, D-amino-acid oxidase and urate oxidase decreased in vitamin E-deficient rats. On the other hand, activities of fatty acyl-CoA oxidase and carnitine acetyltransferase increased significantly in vitamin E-deficient rats. All activities of these peroxisomal enzymes were restored to the control levels in vitamin E-supplemented rats. The activities of the mitochondrial, lysosomal and microsomal enzymes tested showed no apparent change except that the change of mitochondrial palmitoyltransferase was shown to be similar to that of peroxisomal fatty acid oxidation. These results were also supported by cell fractionation techniques. Following the methods of aqueous polymer two-phase systems, the characteristics of peroxisomal surface membranes altered in respect of their hydrophobicity, but not in respect of the surface charge of peroxisomal membranes. These results indicate that peroxisomal functions, especially those of the fatty acid oxidation system, change their activities more sensitively than other intracellular organelles in response to the condition of vitamin E deficiency.
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PMID:Effects of long-term vitamin E deficiency and restoration on rat hepatic peroxisomes. 614 46

Effects of a short-term vitamin E deficiency on some lipid peroxidative properties were investigated in mouse cardiac and skeletal muscles. The concentration of vitamin E decreased 35.8% in 5 weeks and 61.2% in 12 weeks in skeletal muscle. The corresponding decrease in cardiac muscle was 65.7% in 12 weeks. Simultaneously the susceptibility of muscle homogenates to in vitro lipid peroxidation increased with 48.6% (5 weeks) and 44.5% (12 weeks) in skeletal muscle and with 101.8% (12 weeks) in cardiac muscle. Highly significant negative correlations were observed between the concentration of vitamin E and in vitro lipid peroxidation in cardiac and skeletal muscles. Also the sensitivity to Fe2+-induced peroxidation was increased in skeletal muscle after the deficiency of 5 weeks. The total contents of peroxidizable lipids (Fe2+-induction) were significantly (approx. 20%) decreased after 12 weeks in cardiac and skeletal muscles. The concentration of lipofuscin was unaffected in both muscles of vitamin E-deficient mice. Vitamin E deficiency (5 weeks) decreased the activity of selenium-dependent glutathione peroxidase in skeletal muscle but did not affect the activities of catalase and beta-glucuronidase and the concentrations of protein, reduced glutathione and total sulfhydryl groups. These results show that a short-term vitamin E deficiency affects the peroxidative properties of cardiac and skeletal muscles and may thus expose the muscles to peroxidation injuries.
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PMID:Vitamin E deficiency and the susceptibility to lipid peroxidation of mouse cardiac and skeletal muscles. 652 97

Nitro blue tetrazolium (NBT) staining in normal rat retina was previously found to be affected by inhibition of free radical-related enzyme systems, indicating that NBT might be useful as a marker of free radicals. The aim of the present study was to investigate NBT staining in rat retina in vitamin E deficiency and after blue light exposure, and also to measure hydrogen peroxide (H2O2) production indirectly by measuring catalase activity under these conditions. Vitamin E deficiency resulted in morphological changes in the retina and increased NBT staining in the photoreceptors and in the outer plexiform layer. Light exposure caused increased staining in the inner segments of photoreceptors. The increased staining was not clearly influenced by addition of the free radical scavengers superoxide dismutase and catalase. The catalase activity was not influenced by light exposure, while it was increased in vitamin E-deficient retina compared to controls. The results indicate that reducing systems as measured by NBT were activated in the retina under these conditions. However, to what extent the reductants represent free radicals still has to be established using other methods.
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PMID:Nitro blue tetrazolium staining and hydrogen peroxide production in the rat retina in vitamin E deficiency and after light exposure. 751 60

The effects of oxygen inhalation for 48 h on the antioxidant capacity of lungs, livers, and brains in normal and vitamin E-deficient rats at various ages were examined. The activity levels of catalase, glutathione peroxidase, and superoxide dismutase, and the level of vitamin E in tissue homogenates were assayed as the indices of antioxidant capacity. Oxygen inhalation mostly decreased antioxidant enzyme activity in lungs. In particular, the catalase activity was much decreased. The glutathione peroxidase activity tended to be decreased. The superoxide dismutase activity was decreased in 32-month-old rats. Vitamin E deficiency did not augment oxidative damage due to oxygen inhalation. There appears to be no age effect on the oxygen-induced decrease in the antioxidant enzyme activities of lungs, except the superoxide dismutase activity in very old rats. Oxygen inhalation had some effects on the antioxidant capacity of livers and brains. For example, oxygen inhalation decreased the vitamin E concentration of livers in 32-month-old, normal rats. These results suggest that the antioxidant capacity of lungs is directly damaged by oxygen inhalation and that the antioxidant capacity of livers and brains is indirectly affected through lung damage. Antioxidant capacity may be maintained without large variation during young and middle ages, but its redundancy for emergency use may be diminished in old age.
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PMID:Effects of oxygen inhalation on the antioxidant capacity of lungs, livers, and brains in normal and vitamin E-deficient rats at various ages. 761 20

The hepatic and pulmonary effects of nitrofurantoin (40 mg/kg, intraperitoneally) were determined at 4 and 24 hr following its administration in mice fed for 10 weeks with a vitamin E sufficient, deficient or enriched diet. Liver glutathione (GSH) was reduced by nitrofurantoin at 4 hr but was unchanged 20 hr later. Nitrofurantoin did not affect liver glutathione peroxidase, glutathione reductase or superoxide dismutase activities. Liver catalase activities were decreased by nitrofurantoin at 4 hr. Lung GSH levels were increased whilst glutathione peroxidase activity was decreased at 4 and 24 hr. Lung glutathione reductase activity was reduced in certain groups. Nitrofurantoin did not affect lung superoxide dismutase, but catalase was decreased at 24 hr. Liver malondialdehyde levels were increased by nitrofurantoin in the vitamin E deficient group whilst lung malondialdehyde levels remained unchanged. Both liver and lung malondialdehyde levels were unaffected by vitamin E supplementation when compared to the vitamin E-sufficient group. These results suggest that nitrofurantoin (40 mg/kg) was deleterious to the liver and lung. Nitrofurantoin-induced lipid peroxidation was seen in vitamin E deficiency but an increase in dietary vitamin E content did not provide additional protection compared to the recommended daily allowance. The antioxidant activities of alpha-tocopherol and gamma-enriched tocotrienol were similar.
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PMID:Nitrofurantoin-induced hepatic and pulmonary biochemical changes in mice fed different vitamin E doses. 900 Feb 62


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