Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042875 (vitamin E deficiency)
916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dietetic microangiopathy ("mulberry heart disease") is a common disease of weaned pigs in several countries. It is characterised by sudden death and has been associated with vitamin E deficiency. We investigated whether it could be induced by depleting pigs of vitamin E with or without a mild peroxidative challenge. In a 2 x 2 experiment, the effect on pigs of depletion of alpha-tocopherol and supplementation with alpha-tocopherol-stripped corn oil were investigated. Although dietetic microangiopathy was not induced, there was evidence of lipid peroxidation, as judged by increased concentrations of Fe++(-)induced 4-hydroxynonenal (4-HNE) and decreased amounts of linolenic acid (C18:3, omega-3) in tissue. Reduced glutathione (GSH) can conjugate to 4-HNE in an attempt to detoxify this highly toxic compound. GSH concentrations were decreased in skeletal muscle, but not in heart, of pigs that were depleted of alpha-tocopherol with or without supplementation with corn oil. The activity of glucose-6-phosphate dehydrogenase (G6PDH) was higher in heart than in skeletal muscles. It is postulated that sufficient NADPH may be produced in heart to maintain GSH concentrations at a level sufficient to conjugate the excess 4-HNE produced by alpha-tocopherol deficiency and/or oil supplementation.
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PMID:Feeding corn oil to vitamin E-deficient pigs increases lipid peroxidation and decreases tissue glutathione concentrations. 882 97

The male reproductive tract of the Brown Norway rat is profoundly affected by aging. In the epididymis, the site of sperm maturation and storage, aging results in histological and biochemical changes that are suggestive of oxidative stress. Vitamin E is a potent lipid-soluble antioxidant that ameliorates the oxidative stress load associated with some chronic disease conditions. To determine the effects of long-term (18-mo) vitamin E deficiency and supplementation on aging in the epididymis, we assessed gene expression changes using cDNA microarrays and lipid peroxidation using immunohistochemical detection of 4-hydroxynonenal (4-HNE) in 24-mo-old rats. Plasma vitamin E levels were significantly lower in vitamin E-deficient animals and higher in vitamin E-supplemented animals compared with age-matched controls. Vitamin E deficiency resulted in increased expression of oxidative stress-related transcripts along the epididymis. This effect was most marked in the corpus epididymidis, where expression of glutathione S-transferases pi, 8, and mu, as well as superoxide dismutase, increased by over 50%. The effect of vitamin E supplementation on the expression of oxidative stress-related transcripts was primarily decreased expression; however, the magnitude of the gene expression changes was smaller than that observed for vitamin E deficiency. 4-HNE immunostaining was present throughout the epididymis in control animals. Vitamin E deficiency both increased the intensity and altered the distribution of 4-HNE staining, while vitamin E supplementation had no observable effect. In summary, we found that long-term vitamin E treatment alters the expression of oxidative stress-related transcripts. Moreover, long-term vitamin E deficiency exacerbates the effects of age on the accumulation of oxidative stress damage in the epididymis.
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PMID:The effects of long-term vitamin E treatment on gene expression and oxidative stress damage in the aging Brown Norway rat epididymis. 1517 34