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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

In AUG rats, deprived of vitamin E for 90 days, we noted a 3-fold increase of kinetic parameters of luminol-dependent chemiluminescence of macrophages, stimulated with opsonized zymosan, superoxide dismutase activity decrease and increment of plasma membrane lipid bilayer microviscosity, which was estimated by fluorescent probe pyrene eximerization method. Vitamin E deficiency did not affect glutathione peroxidase and glutathione reductase activities of macrophages.
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PMID:Effect of vitamin E deficiency on oxidative metabolism and antioxidant enzyme activity of macrophages. 240 45

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

Doxorubicin induces an acute cardiotoxicity that becomes manifest in isolated hearts as a deterioration in mechanical function. The oxidative component in this myocardial damage has been investigated. The effects of doxorubicin on the activity of superoxide dismutase and the capacity of the glutathione system, factors of the cellular protective mechanism against free radicals, were examined in rat isolated heart. Doxorubicin was found to reduce the capacity of the protective mechanisms. Whether oxidative membrane damage due to excessive free radical formation plays a role in the pathogenesis of the acute cardiotoxic action of doxorubicin was also examined. Its acute effect on myocardial contraction amplitude, frequency of beating, coronary flow and on the above mentioned biochemical parameters was compared in rat hearts sufficient or deficient in vitamin E. Peroxidation of lipids was measured as the formation of malondialdehyde, one of the final products of this process. Vitamin E deficiency neither aggravated the decrease in the capacity of the cellular protective factors nor worsened the reduction in myocardial function. Nor did induction of lipid peroxidation by doxorubicin occur in vitamin E-deficient hearts. It was concluded that lipid peroxidative damage most probably is not decisive in the development of the acute cardiomyopathy in rats.
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PMID:The role of lipid peroxidation in acute doxorubicin-induced cardiotoxicity as studied in rat isolated heart. 287 91

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

After 2 month of feeding vitamin E-supplemented diet (100.6 and 0 mg/kg; group I-control, II and III, respectively) the concentration of lipid peroxidation products (diene conjugates, malondialdehyde, Schiff's bases) and activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) was estimated in rat heart and liver. Although the content of alpha-tocopherol in organs of group II was significantly decreased, the concentration of peroxidation products and enzyme activities was unchanged. Moreover, these parameters were constant in rat liver of group III. The heart was more sensitive because in group III to vitamin E deficiency (the alpha-tocopherol level was dropped fourfold) the concentration of diene conjugates and malondialdehyde was increased and superoxide dismutase activity was decreased. Thus insufficiency of vitamin E may result in selective alterations of myocardial functions. In addition, vitamin E may be useful instrument for correction of free radical oxidation and antioxidant system activity in the heart.
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PMID:[The content of lipid peroxidation products and the activity of antioxidant enzymes in the myocardium and liver of rats with various vitamin E allowances]. 320 72

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

In 1969 McCord and Fridovich discovered superoxide dismutase, which converts the oxygen free radical O(2) (-) to hydrogen peroxide H(2)O(2). In the presence of excess O(2) (-), H(2)O(2) may then undergo further reduction to the highly toxic hydroxyl radical, OH(*). Since the description of this enzymatic process, there has been explosive growth in related biochemical research, which has now percolated through to clinical investigation. The hypoxanthine-xanthine oxidase system originally used as a radical production model has a close counterpart in the ischemia-reperfusion phenomenon purported to cause diseases of heart, brain and gastrointestinal tract, and free radicals are now known to have a critical role in postphagocytic bacterial killing. Prototypic deficiency diseases such as chronic granulomatous disease are now recognized. Some evidence indicates that excess states such as perhaps Batten's disease also occur, and environmental influences such as selenium and vitamin E deficiency may augment free radical levels. Many disorders including microvasculopathies, noncardiogenic pulmonary edema, glomerulopathies and radiation damage may owe part of their proximate pathogenesis to free radicals. Control of tissue free radical levels is now pharmacologically feasible and perhaps justified for specific diseases.
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PMID:The expanding role of oxygen free radicals in clinical medicine. 352 Oct 94

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

The effects of vitamin E deficiency and excess polyunsaturated acids in the diet on luminol-dependent chemiluminescence were studied in Aug-Lac rats. It was chown that experimental prooxidant regiments led to the increase of oxidative metabolism in macrophages stimulated by opsonized zymozan. Vitamin E deficient regimens decreased superoxide dismutase activity of macrophages. In vitro DL-alpha-tocopherol and the synthetic antioxidants BHT and BHA inhibited chemiluminescence of macrophages. Arachidonic acid activated macrophages and induced the formation of oxygen radicals.
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PMID:[Effect of pro- and antioxidant food factors on macrophage oxidative metabolism]. 403 77


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