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)

1. Male rats were deprived as weanlings of dietary vitamin E for 2, 4, 6, 10 and 12 months. Mesenteric arterial beds from these rats and from age-matched controls were isolated and perfused with Krebs solution at a constant flow rate (5 ml min-1). The function of perivascular sympathetic nerves, smooth muscle and endothelium was assessed. 2. At 12 months vitamin E deficient rats exhibited the characteristic symptoms of vitamin E deficiency, namely poor coat condition, muscle wasting, kyphoscoliosis and impaired gait. In the isolated mesenteric arterial bed electrical field stimulation (EFS) of perivascular nerves (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent vasoconstrictor responses which were unaffected by vitamin E deficiency except at 12 months, at which age responses were significantly greater than those of the controls at 24 and 32 Hz (P < 0.01). 3. Exogenous noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent vasoconstriction which was similar in vitamin E-deficient and control preparations at all ages. Potassium chloride (0.15 mmol) also produced similar vasoconstrictor responses in vitamin E-deficient and control preparations at each age. 4. Tone of the preparations was raised by continuous perfusion with methoxamine (4-70 microM), producing similar increases in perfusion pressure in vitamin E-deficient and control preparations at each age. Endothelium-dependent dose-dependent vasodilatation to adenosine 5'-triphosphate was significantly impaired in mesenteric arterial beds from 12 month-old vitamin E-deficient rats compared with the controls (P < 0.05). Relaxation to acetylcholine was not significantly different at any age. 5. Endothelium-independent vasodilatation to sodium nitroprusside was similar in vitamin E-deficient rats and age-matched controls. 6. These results suggest that long term (12 months) deprivation of dietary vitamin E may impair endothelial function in mesenteric arteries of the rat. Sympathetic perivascular nerve constrictor function was increased at 12 months. There were no functionally expressed changes in the vascular smooth muscle, which appears to be more resilient to the effects of oxidative stress in vitamin E deficiency.
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PMID:Effects of chronic vitamin E deficiency on vascular function--a study of sympathetic nerves, smooth muscle and endothelium of the mesenteric arterial bed of the rat. 868 Jul 33

1. Male rats were deprived as weanlings of dietary vitamin E and fed on a high polyunsaturated fatty acid (PUFA) diet for 6 months. Rats fed on a high PUFA or on an untreated diet served as controls. Mesenteric arterial beds were isolated and perfused at a constant flow rate (5 ml min-1) and the function of sympathetic nerves, smooth muscle and endothelium was assessed. 2. Electrical field stimulation (4-32 Hz, 90 V, 1 ms, for 30 s) elicited frequency-dependent vasoconstriction of the mesenteric arterial preparations. Response curves were similar between untreated control and PUFA-fed control groups. Maximum vasoconstrictor responses (at 24 and 32 Hz) were significantly attenuated in rats deprived of vitamin E and on a high PUFA diet compared to the PUFA-fed controls (P < 0.05). 3. Exogenous noradrenaline (NA; 0.15-500 nmol) elicited dose-dependent constriction of the mesenteric arterial beds. Preparations from rats fed on a high PUFA diet elicited significantly smaller responses compared to the control group. There was no significant difference in constrictor responses of PUFA rats deprived of vitamin E compared to the PUFA controls. Vasoconstrictor responses to doses of adenosine 5'-triphosphate (ATP) (5-5000 nmol) were significantly impaired in vitamin E-deficiency with a high PUFA diet compared to a high PUFA diet alone (P < < 0.001). Constrictor responses to potassium chloride (0.15 mmol) were significantly impaired in vitamin E-deficient PUFA rats compared to the PUFA-fed control group (P < 0.05). 4. Vasodilator responses were assessed in preparations in which tone was raised by continuous perfusion with methoxamine (4-25 microM). Mesenteric arterial beds from PUFA-fed rats deprived of vitamin E acquired significantly less tone, 59.8 +/- 4.6 mmHg (n = 7), than PUFA-fed controls 116.9 +/- 7.6 mmHg (n = 7) (P < 0.001) and were refractory to further increases in tone with further additions of methoxamine. Methoxamine-induced tone of PUFA-fed controls was greater than in P that in the untreated controls (83.9 +/- 7.4 mmHg; n = 5) (P < 0.05). Responses to the endothelium-dependent vasodilators acetylcholine (ACh) and ATP were significantly reduced in preparations from rats fed on the vitamin E-deficient high-PUFA diet compared to PUFA controls. Vasodilator responses to ACh were greater in PUFA controls than in untreated controls and this reached statistical significance at 5 nmol ACh. 5. Vasodilator responses to sodium nitroprusside, which acts directly on the vascular smooth muscle, were similar in untreated control and PUFA control groups. Responses were significantly attenuated in vitamin E-deficient PUFA rats compared to the PUFA control group (P < < 0.001). 6. These results indicate that a combination of a high PUFA diet and vitamin E deficiency impairs mesenteric arterial function at the level of the vascular smooth muscle. A high PUFA diet alone attenuates responses to NA and augments endothelium-dependent vasodilation. The detrimental effects of loss of antioxidant activity due to vitamin E-deficiency on vascular function may be exacerbated by a high PUFA diet.
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PMID:Effects of chronic vitamin E deficiency and a high polyunsaturated fatty acid diet on rat mesenteric arterial function. 868 Jul 46

Marked electrolyte abnormalities characterized by profound hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia were noted in 4 neonatal foals with acute rhabdomyolysis and pigmenturia. In 2 foals, rhabdomyolysis developed 4-6 days after admission for dysmaturity, and in 2 foals, rhabdomyolysis was evident on presentation. Rhabdomyolysis was a consequence of selenium deficiency with or without vitamin E deficiency, possibly combined with increased oxidant stress due to sepsis or hypoxia and reperfusion injury after parturition. Foals gained from 7 to 15% of their initial body weight within 48 hours of developing rhabdomyolysis. Three of the foals developed cardiac arrhythmias characterized by spiked T waves and decreased-amplitude P waves. Postmortem examination of 2 foals revealed extensive myodegeneration and renal tubular nephrosis; renal cortical necrosis with myocardial necrosis was noted in 1 foal. Destruction of the major intracellular compartment (intracellular fluid [ICF]) through extensive myonecrosis combined, in some cases, with myoglobinuric renal insufficiency produced major fluid shifts and life-threatening electrolyte derangements. With the major ICF compartment disrupted, hyperkalemia was most effectively treated using mineralocorticoids, loop diuretics, and ion exchange resins to enhance elimination. In addition, i.v. calcium, glucose, insulin, and sodium bicarbonate were administered, which helped redistribute potassium to the ICF. Severe rhabdomyolysis should be included in the differential diagnoses of hyperkalemia, hyponatremia, hypocalcemia, and hyperphosphatemia in neonatal foals.
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PMID:Electrolyte disturbances in foals with severe rhabdomyolysis. 959 79

Plasma concentrations of alpha-tocopherol (vitamin E) and other analytes in Asian elephants (Elephas maximus) in Nepal were determined during typical work camp management of the elephants. Elephants foraged for food for 4-6 hr each day under the control of mahouts and were also provided daily with cut forage and supplements of unhusked rice, cane molasses, and salt. Blood samples were taken monthly for 1 yr without chemical restraint from 26 female elephants in four camps. Elephants were 6-60+ yr of age. Mean (+/-SEM) alpha-tocopherol concentration was 0.77+/-0.047 microg/ml, with a range of 0.23-1.57 microg/ml. Subadults had lower concentrations than did older elephants, and there were significant differences in mean concentrations from different camps and in mean monthly concentrations. Plasma alpha-tocopherol concentration appears to vary widely between individuals, and a single value of <0.3 microg/ml is not sufficient to diagnose incipient vitamin E deficiency. Mean (+/-SEM) plasma retinol (vitamin A) concentration was 0.063+/-0.003 microg/ml with a range of 0.01-0.12 microg/ml. Subadults had higher concentrations than did older elephants, and mean retinal values differed significantly among camps. Beta-carotene was not found in plasma. Twenty-five other analytes determined or derived were generally similar to those reported in other Asian and African (Loxodonta africana) elephants. Estimates of nutrient intake, based upon diet composition, suggested that dietary concentrations of zinc and sodium may have been marginal, but the absence of signs of any nutrient deficiencies indicates that dietary husbandry in these elephant camps was generally satisfactory.
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PMID:Plasma vitamin E and other analyte levels in Nepalese camp elephants (Elephas maximus). 980 97

Our objective was to determine whether high levels of dietary vitamin E replaced the protection of the Se-dependent cellular glutathione peroxidase (GPX1) against paraquat- or diquat-induced acute oxidative stress in mice. Two experiments were conducted using GPX1 knockout [GPX1(-/-)] mice and wild-type (WT) mice (n = 78/group). In Experiment 1, mice were fed torula yeast-based, Se-adequate (0.4 mg/kg as sodium selenite) diets + 0, 75, 750 or 7,500 mg all-rac-alpha-tocopheryl acetate for 5 wk before an intraperitoneal injection of 50 mg paraquat/kg body weight. In Experiment 2, mice were fed the diet + 0 or 750 mg all-rac-alpha-tocopheryl acetate for 5 wk and were killed 1 or 3 h after an injection of diquat at 12, 24 or 48 mg/kg. In Experiment 1, all mice died of the injection and there were 8- to 15-fold differences (P < 0.001) in survival times between the GPX1(-/-) and the WT mice. Although increasing tocopheryl acetate from 0 to 750 mg/kg extended the survival time of the GPX1(-/-) mice for 2 h (P = 0.06), the highest tocopheryl acetate level resulted in a decrease (P < 0.05) in survival time in the WT mice. The vitamin E-deficient GPX1(-/-) mice had the highest concentration of hepatic thiobarbituric acid reacting substances. In Experiment 2, the diquat-induced formation of hepatic F(2)-isoprostanes was accelerated (P < 0.05) by vitamin E deficiency and was also affected by the GPX1 knockout. Diquat produced much greater (P < 0.01) dose-dependent increases in plasma alanine transaminase (ALT) activities in the GPX1(-/-) than in the WT mice. Hepatic phospholipid hydroperoxide GPX activities were decreased (P < 0.05) by the diquat injection only in the vitamin E-deficient GPX1(-/-) mice. Despite a potent inhibition of hepatic lipid peroxidation, high levels of dietary vitamin E do not replace the protection of GPX1 against the paraquat-induced lethality or the diquat-induced plasma ALT activity increase in mice.
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PMID:High levels of dietary vitamin E do not replace cellular glutathione peroxidase in protecting mice from acute oxidative stress. 1053 68


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