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

The vitamin E (alpha-tocopherol) and free and bound malondialdehyde (MDA) in ventricular heart muscle and myocardial membrane from Wistar-Kyoto (W/K) normotensive and spontaneously hypertensive (SH) rats have been measured directly by high performance liquid chromatography (HPLC). Thiobarbituric acid-reactive substance (TBA-RS) in the myocardium and heart-muscle membrane of the two strains was also quantified by a colorimetric TBA test. It was found that SH-rat myocardium and myocardial membrane contained more than 3-fold less alpha-tocopherol than did heart muscle and cardiac membrane of the normotensive rat. Coincident with this relative vitamin E deficiency were several-fold greater amounts of MDA and TBA-RS in SH-rat myocardium and myocardial membrane. Most (87%) of the MDA in SH-rat heart muscle, but only 40% in W/K-rat heart muscle, was free (i.e., unbound). These results offer direct evidence that SH-rat myocardium is vitamin E-deficient and highly peroxidative, relative to cardiac muscle of the normotensive W/K parent strain. The lower vitamin E content of SH-rat myocardium is particularly striking, because SH-rat myocardial membrane was found to contain approximately 35% more phospholipid than myocardial membrane in the W/K rat. Although the amounts of myocardial TBA-RS are greater in the SH strain, they do not reflect the actual MDA profiles of the heart muscles or the heart membranes and cannot be used as a quantitative index of cardiac oxidative-injury status due to non-MDA TBA-RS in both strains.
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PMID:Cardiac membrane vitamin E and malondialdehyde levels in heart muscle of normotensive and spontaneously-hypertensive rats. 274 28

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

Oxidative damage and the role of antioxidants and prooxidants in aerobic metabolism is of great current interest; it spans areas of research such as carcinogenesis, ageing, toxicology and nutrition. We have used Bantin-Kingman female rats for both in vivo and in vitro studies. In these animals we have altered the levels of all-rac-alpha-tocopherol (vitamin E) by dietary means and have used physical exercise and visible light exposure to alter oxidative stress. Our results show a progressive and specific increase in the susceptibility of many subcellular membranes to oxidative damage with increasing levels of vitamin E deficiency and/or physical stress. In addition, endurance training raised the levels of antioxidative enzymic pathways in both skeletal and cardiac muscle.
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PMID:Vitamin E, physical exercise and tissue oxidative damage. 655 8

A case of fatal familial intrahepatic cholestasis (Byler disease) developed a neuromuscular syndrome similar to that in experimental vitamin E deficiency and abetalipoproteinemia, and died of hepatic and cardiac failure. Serum vitamin E level was extremely low. Autopsy revealed intrahepatic cholestatic cirrhosis without obliterative lesions in the bile duct system and marked splenomegaly with splenoma-like nodules. The other pathological lesions were considered to be due to chronic vitamin E deficiency as follows:1. Mitochondrial changes especially of the hepatocyte and cardiac muscle. 2. Cardiomyopathy. 3. Myopathy. 4. Vasculopathy. 5. Systemic lipofuscinosis. 6. Lesions of the reproductive and endocrine organs. 7. Kyphoscoliosis and pes cavus. 8. Systemic neuroaxonal dystrophy with peripheral neuropathy.
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PMID:Pathology of chronic vitamin E deficiency in fatal familial intrahepatic cholestasis (Byler disease). 713 26

Over a period of 4 wk, 24 10-d-old broiler hens were fed diets containing 11% vegetable oil (9% rapeseed oil, 2% soybean oil), which was added either fresh (1 meq O2/kg oil) or oxidized (156 meq O2/kg oil). The effects of the dietary treatments on nutrient digestibility were examined in a balance experiment. The antioxidative status of the animals was evaluated using plasma concentrations of thiobarbituric acid-reactive substances (TBARS), erythrocyte hemolysis in vitro, selenium-dependent and selenium-independent activity of glutathione peroxidase in liver cell cytosolic fractions, and concentrations of tocopherols and other fat-soluble compounds with antioxidative properties (lutein, beta-carotene, and retinol) in plasma and various tissues (skeletal muscle, cardiac muscle, liver, and abdominal fat). Compared to the fresh oil, the concentrations of linoleic and linolenic acid were slightly lower in oxidized oil. The concentration of alpha-tocopherol in the diet with fresh oil was an average of 80.8 mg/kg diet, whereas the diet with oxidized oil only provided 44 mg/kg. The dietary selenium content averaged 0.48 mg/kg in both diets. During the experiment, none of the animals showed symptoms of diarrhea or vitamin E deficiency. The intake of oxidized oil caused a growth depression after 2 wk. The retention of fat (P = 0.07), energy (P = 0.09), and alpha-tocopherol (P < 0.01) was lower in the group fed oxidized fat. Furthermore, these animals showed significantly higher plasma concentrations of TBARS (P < 0.01), and lower concentrations of tocopherols, lutein, beta-carotene, and retinol in plasma and tissues.
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PMID:Inclusion of oxidized vegetable oil in broiler diets. Its influence on nutrient balance and on the antioxidative status of broilers. 882 33