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

It is well known that vitamins E and C exhibit synergistic action in in vitro systems, but with regard to in vivo systems, much of the available data are confusing. To elucidate this problem we used a new mutant of Wistar-strain rats that cannot synthesize vitamin C, namely, ODS rats. Two experiments were planned: (1) during development of vitamin E deficiency, whether vitamin C could spare the consumption of vitamin E; and (2) under conditions of a regular level of vitamin E intake, whether different dose levels of vitamin C can affect vitamin E concentration in tissues. The results obtained show that with vitamin C intake, higher levels of vitamin E were deposited in tissues in both experiments. With the development of vitamin E deficiency, rats in the group with a higher dose of vitamin C deposited higher concentrations of alpha-tocopherol. With simultaneous administration of vitamin E and vitamin C to the same mutant rats, the rats in the group with a higher dose of vitamin C deposited higher levels of vitamin E in all tissues tested. Thus, we concluded that vitamin C can spare the consumption of vitamin E in vivo as well as in vitro.
 ...
PMID:Synergistic action of vitamin E and vitamin C in vivo using a new mutant of Wistar-strain rats, ODS, unable to synthesize vitamin C. 176 40

Effects of dietary vitamin E deficiency on the fatty acid compositions of total lipids and phospholipids were studied in several tissues of rats fed a vitamin E-deficient diet for 4, 6, and 9 months. No significant differences were observed between the vitamin E deficiency and controls except in the fatty acid profiles of liver total lipids. Triacylglycerol (TAG) accumulation was found in the liver of rats fed a vitamin E-deficient diet. The levels of TAG-palmitate and -oleate increased particularly in the liver from such animals. The fatty acid compositions of hepatic phospholipids were not affected by the diet. Increased TAG observed in the liver of rats fed a vitamin E-deficient diet was restored to normal when the diet was supplemented with 20 mg alpha-tocopheryl acetate/kg diet. These findings indicate that dietary vitamin E deficiency causes TAG accumulation in the liver and that the antioxidant, vitamin E, is capable of preventing free radical-induced liver injury.
 ...
PMID:Free radical-induced liver injury. I. Effects of dietary vitamin E deficiency on triacylglycerol level and its fatty acid profile in rat liver. 177 4

Fat-soluble vitamin status was assessed in 36 infants diagnosed with cystic fibrosis by newborn screening in the Colorado Program. At the time of diagnosis of cystic fibrosis, 36% of infants were hypoalbuminemic, 21% had vitamin A deficiency, 35% had vitamin D deficiency, and 38% had vitamin E deficiency. None had vitamin K deficiency. Supplementation with pancreatic enzymes, a multiple vitamin preparation, and additional vitamin E was associated with normalization of serum albumin, retinol, and 25-hydroxyvitamin D and negative PIVKA testing at age 6 and 12 months. Several patients remained vitamin E deficient, but this was felt to be due to poor compliance. Biochemical evidence of fat-soluble vitamin deficiency is common before age 3 months in infants with CF and responds to supplementation in the first year of life.
 ...
PMID:Fat-soluble vitamins in infants identified by cystic fibrosis newborn screening. 178 31

Nerve tissue (as well as capillaries and cerebral microvessels) has a very high concentration in polyunsaturated fatty acids belonging to linoleic and alpha-linolenic series. Nerve tissue also requires large amounts of oxygen. Radical peroxidation of the polyunsaturated fatty acids represents a serious risk to the biochemistry and physiology of the membranes: it can be a cause of cellular death. During aging, the capillaries and cerebral microvessels undergo extensive modifications at the level of the polyunsaturated fatty acids: for example, the concentration of arachidonic acid decreases by half. In brain in general, vitamin E is very well protected: after oxidation, it is rapidly regenerated; it seems to undergo only slight degradation. In case of dietary deficiency, the brain loses much less vitamin E, and at a slower rate, than other non-nerve tissue. During aging, there is a relation between the content in vitamin E and the concentration of polyunsaturated fatty acids of the linoleic series, but not of the alpha-linolenic series. In addition, vitamin E deficiency also leads to a decrease in the enzymatic activities that protect against peroxidation of fatty acids.
 ...
PMID:[Vitamin E: protection of membrane polyunsaturated fatty acids against radical peroxidation in the course of cerebral aging, particularly in cerebral capillaries and microvessels]. 180

Vitamin E includes eight naturally occurring fat-soluble nutrients called tocopherols and dietary intake of vitamin E activity is essential in many species. alpha-Tocopherol has the highest biological activity and the highest molar concentration of lipid soluble antioxidant in man. Deficiency of vitamin E may cause neurological dysfunction, myopathies and diminished erythrocyte life span. alpha-Tocopherol is absorbed via the lymphatic pathway and transported in association with chylomicrons. In plasma alpha-tocopherol is found in all lipoprotein fractions, but mostly associated with apo B-containing lipoproteins in man. In rats approximately 50% of alpha-tocopherol is bound to high density lipoproteins (HDL). After intestinal absorption and transport with chylomicrons alpha-tocopherol is mostly transferred to parenchymal cells of the liver were most of the fat-soluble vitamin is stored. Little vitamin E is stored in the non-parenchymal cells (endothelial, stellate and Kupffer cells). alpha-Tocopherol is secreted in association with very low density lipoprotein (VLDL) from the liver. In the rat about 90% of total body mass of alpha-tocopherol is recovered in the liver, skeletal muscle and adipose tissue. Most alpha-tocopherol is located in the mitochondrial fractions and in the endoplasmic reticulum, whereas little is found in cytosol and peroxisomes. Clinical evidence from heavy drinkers and from experimental work in rats suggests that alcohol may increase oxidation of alpha-tocopherol, causing reduced tissue concentrations of alpha-tocopherol. Increased demand for vitamin E has also been observed in premature babies and patients with malabsorption, but there is little evidence that the well balanced diet of the healthy population would be improved by supplementation with vitamin E.
 ...
PMID:Absorption, transport and metabolism of vitamin E. 187 54

The effects of vitamin E on toxicity by minute amounts of paraquat fed continuously for some period to rats were investigated. Two experiments were carried out as experiments 1 and 2. In both experiments, weaning rats were divided at first into two groups; one group was given a vitamin E-deficient diet, and the other a vitamin E-supplemented control diet (50 mg alpha-tocopherol/kg of diet). They were fed on these diets for 40 days. After that, in both experiments, the rats that had been fed the vitamin E-deficient diet were further divided into two groups, which were either given a paraquat-added diet (+PQ-E) or continuously fed the same vitamin E-deficient diet (-E). The amount of paraquat added was 250 mg of methyl viologen per kg of diet. After the addition of paraquat, these two groups were pair-fed. In experiment 1, paraquat was given to all the rats fed the vitamin E-supplemented control diet (+PQ+E). In experiment 2, rats fed the control diet were divided into paraquat-added (+PQ+E) and non-paraquat-added (+E) groups, similar to those of vitamin E-deficient rats. These two groups were also pair-fed thereafter. In both experiments, about 35 days after paraquat addition, they were sacrificed. Plasma and liver alpha-tocopherol contents were measured by HPLC, and liver peroxidation value was measured by chemiluminescence and the TBA method. And, as parameters of vitamin E deficiency, plasma pyruvate kinase and GOT activities and alpha-cysteine proteinase inhibitor (alpha-CPI) level were measured. When the analyzed values were compared between paraquat-added and the corresponding not-added control groups (+PQ-E vs. -E, +PQ+E vs. +E), the following results were obtained. In experiment 1, the values of plasma and liver alpha-tocopherol levels were significantly lower in the +PQ-E group than those of the -E group; however, liver peroxidation values and values of the three parameters of vitamin E deficiency were not different significantly. In experiment 2, the value of liver alpha-tocopherol level was significantly lower in the +PQ+E group than that of the +E group.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Effects of vitamin E on toxicity by minute amounts of paraquat fed continuously to rats. 188 Jun 28

Four-week-old Wistar male rats were fed a vitamin E (VE)-deficient (0E) or a VE-sufficient (10E) diet for 6 weeks and then intraperitoneally treated with buthionine sulfoximine (BSO) at 1 mmol/kg body weight once a day for 3 days. Glutathione (GSH) depletion by BSO treatment caused injuries especially in the kidneys of VE-deficient rats. The kidney weight increased in the VE-deficient rats after BSO treatment (0E-BSO). It was observed that the epithelial cells of the renal tubules in this group were strongly impaired and the injuries were necrosis and desquamation. No injury was observed in the kidneys of the BSO-untreated 0E group and the 10E groups. The TBA value of the kidney of 0E-BSO group was lower than that of the BSO-untreated 0E group, but the lipofuscin content of the kidney of the 0E-BSO group was 10 times higher than that of the BSO-untreated 0E group. These results suggest that the kidney injuries in rats may be caused by lipid peroxidation induced by vitamin E deficiency and glutathione depletion.
 ...
PMID:Kidney injury induced by lipid peroxide produced by vitamin E deficiency and GSH depletion in rats. 188 Jun 35

Sixty crossbred (Yorkshire-Hampshire X Duroc) gilts were fed one of four corn-soybean meal diets fortified with .3 ppm Se and 0, 16, 33, or 66 IU of DL-alpha-tocopheryl acetate/kg. The study was conducted over a three-parity period to evaluate sow reproductive performance and the vitamin E tissue status of both sows and progeny at various time periods postcoitum and(or) postpartum. The basal diet averaged 8.4 mg of alpha-tocopherol/kg and .38 ppm of Se. Although litter size at birth was lowest (P less than .15) when sows were fed the basal diet, a higher incidence of agalactia when sows were fed the lower dietary vitamin E levels resulted in an increased (P less than .05) litter size at 7 d postpartum as dietary vitamin E increased. Sow serum alpha-tocopherol increased (P less than .01) at each measurement period as dietary vitamin E level increased. Colostrum and milk alpha-tocopherol concentrations increased (P less than .01) as dietary vitamin E level increased, and colostrum values were three to five times higher than at later milks. Colostrum alpha-tocopherol declined by parity from sows fed less than or equal to 16 IU/kg but was similar at each parity for sows fed greater than or equal to 33 IU/kg, resulting in a dietary vitamin E x parity interaction (P less than .01). The Se content of sow milk declined with parity but was not affected by dietary vitamin E level. Sow liver tocopherol at weaning (28 d postpartum) increased (P less than .01) as dietary vitamin E increased and increased with parity (P less than .05). Pig serum and liver alpha-tocopherol concentrations were elevated at birth and 7 and 28 d of age as sow dietary level of vitamin E increased. Upon weaning, pigs were fed a torula yeast-dextrose diet that contained 3.0 mg of alpha-tocopherol/kg and .32 ppm Se for a 28-d postweaning period. Liver and serum alpha-tocopherol concentrations declined during the postweaning period. Evidence of the vitamin E deficiency occurred at 28 d postweaning in the progeny from sows fed the basal diet or 16 IU of vitamin E; the incidence was more prevalent in the pigs from Parities II and III. These results suggest that a supplemental level of 16 IU of vitamin E/kg of diet was inadequate for the reproducing sow; higher levels are justified, particularly when females are retained in the herd for several parities.
 ...
PMID:Assessment of the influence of dietary vitamin E on sows and offspring in three parities: reproductive performance, tissue tocopherol, and effects on progeny. 188 99

Even though vitamin E may not improve physical achievements in sports competitions, as shown in several swimming experiments, it is important for the health of skeletal muscle: in its role as the major lipid-soluble chainbreaking antioxidant in lipid cell membranes, vitamin E protects muscle tissue in aerobic exercise, in which oxygen metabolism and, consequently, free radical production are greatly accelerated. Animal studies in several laboratories have shown that endurance exercise results in the same type of oxidative muscle damage as does vitamin E deficiency: there is an increase in the peroxidation products pentane and malondialdehyde and in enzymes leaked from muscles to plasma. Oxidative tissue damage in vitamin-E deficient animals is exacerbated by endurance training and, conversely, it is reduced by high-dose vitamin E supplementation; also, preliminary studies in humans have demonstrated antioxidant protection by high-dose vitamin E supplementation. After endurance exercise leakage of enzymes into the plasma and output of pentane in the breath were significantly reduced. During a high-altitude expedition in the Himalayas, protection was shown to be significantly better in the supplemented group than in the placebo group, as determined by anaerobic threshold and pentane exhalation.
 ...
PMID:Function of vitamin E in physical exercise: a review. 189 77

The effects of dietary vitamin E and beta-carotene were studied on enzymes involved in arachidonic acid metabolism and other related enzymes in the rat testis. Groups of rats were fed various soybean oil-based semi purified diets. Group 1 was fed a vitamin E-supplemented diet (+E - beta); Group 2 was fed a beta-carotene-supplemented diet (-E + beta); Group 3, the control group (-E - beta) was fed a vitamin E-deficient diet; and Group 4, the standard diet group (S), was fed vitamin E plus beta-carotene-standard diet. Soybean oxidized oil was added to the three diet groups - (+E - beta), (- E + beta) and (- E - beta), whereas the diet of S group contained non-oxidized oil. After 8 weeks rats were killed, blood and testis samples were collected for biochemical determinations. Vitamin E deficiency caused significant increase in testis thiobarbituric acid value and activities of testis NADPH oxidase, testis 15-lipoxygenase and in plasma pyruvate kinase. In contrast, significant decreases were observed in activity of testis prostaglandin synthetase, compared with antioxidant-supplemented diet groups. We also found a significant increase in 15-lipoxygenase activity in (- E + beta) diet group, compared with (- E - beta) diet group. Fatty acid analysis of testis parenchyma indicated decrease in palmitate (16:0) and arachidonate (20:4(n - 6)), and increase in oleate (18:1(n-6)) linoleate (18:2(n - 6)) and linolenate (18:3(n - 3)), when compared (-E - beta) diet group with vitamin E-supplemented diet groups. The results suggest that dietary vitamin E has a role in both enzymatic and non-enzymatic peroxidation of polyunsaturated fatty acids in the testis.
 ...
PMID:The effect of dietary vitamin E and beta-carotene on oxidation processes in the rat testis. 190 Dec 24


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>