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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 deficiency in the rat diet was studied for its effect on the activity of Ca2+-pump and phosphorylation of sarcoplasmic reticulum membrane fragments of myocardium. It is shown that under such an antioxidant deficiency ATP-dependent accumulation of calcium is 2.5 times as low, from 490 down to 190 nmol/mg of protein for 5 min. The administration of ionol, a synthetic antioxidant, to animals reduces the level of calcium accumulation, it is 1.8 times as high as that with vitamin E deficiency; cAMP-dependent phosphorylation of the sarcoplasmic reticulum preparation membranes of the test animal myocardium produces a 1.6-2.1 times increase in them of the ATP-dependent accumulation of calcium, the kinetics of Ca2+ accumulation is unchanged.
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PMID:[ATP-dependent calcium transport in the sarcoplasmic reticulum of the myocardium during vitamin E deficiency in the rat diet]. 284 7

August male rats were kept for 90 days on one of the following diets: balanced semisynthetic diet with casein as a source of protein (group 1), amino acid balanced diet with casein replaced by gluten (group 2), a diet with excess of polyunsaturated fatty acids (group 3), with vitamin E deficiency (group 4), and polyunbalanced diet, comprising a combination of amino acid imbalance, excess of polyunsaturated acids, and vitamin E deficiency (group 5). Structural and functional parameters of Ca2+ transport (Ca2+ accumulation rate, activity of Ca2+-ATPase, Ca/ATP ratio), content of lipid fractions and accumulation of malonic dialdehyde were studied in sarcoplasmatic reticulum (SR) fragments from rat hind limb muscles in the course of ascorbate-dependent lipid peroxidation. Reduction of Ca2+ absorption rate, Ca2+-ATPase, and Ca/ATP ratio in SR membranes were observed in groups 2-5. In parallel, decreased phospholipid and triglyceride levels and increased content of free fatty acids and cholesterol in SR membranes were established.
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PMID:[Action of pro-oxidant diets on the enzymatic system of Ca2+ transport in the sarcoplasmic reticulum]. 409 Apr 4

The role of lipid peroxidation (LPO) in the damages of the enzymic system of Ca2+ transport in sarcoplasmic reticulum (SR) membranes of skeletal and cardiac muscles under conditions of vitamin E deficiency, ischemia and limb reoxygenation as well as in emotional-pain stress was investigated. It was shown that these processes are associated with activation of endogenous LPO in SR membranes "in vivo" and with simultaneous inhibition of Ca2+ transport, (i. e. decrease of the Ca2+/ATP ratio) and inactivation of Ca-ATPase. The degree of damage of the Ca2+ transport system was correlated with the concentration of LPO products accumulated in SR membranes "in vivo and during LPO induction by the Fe2+ + ascorbate system 'in vitro". Injection of natural and synthetic free radical scavengers (e. g. 4-methyl-2.6-ditretbutylphenol, alpha-tocopherol) to experimental animals resulted in practically complete suppression of LPO activation "in vivo" and in partial protection of the Ca2+-transporting capacity of SR membranes. A comparison of experimental results allowed to estimate the role of LPO in SR damage under pathological conditions. Model experiments with "contraction-relaxation" cycles including isolated components of muscle fibers (SR fragments and myofibrils) demonstrated that LPO induction in SR membranes by the Fe2+ + ascorbate system results in complete elimination of the relaxation step in myofibrils due to the loss of the SR affinity to decrease the concentration of Ca2+ in the incubation medium. This effect can be removed by free radical scavengers. The role of LPO in pathological changes of muscle contractility is discussed.
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PMID:[Modification of an enzymic system of Ca2+ transport in sarcoplasmic reticulum during lipid peroxidation. In vivo damages in the development of pathological changes]. 622 70

1. Modified sucrose-gap, standard organ-bath techniques and transmitter release studies were used to examine neuromuscular transmission in the caecum, vas deferens and urinary bladder in normal rats and in rats maintained for 12 months on a diet free of vitamin E. 2. In the caecum circular muscle, non-adrenergic, non-cholinergic inhibitory junction potentials were absent from 48 and 15% of preparations from vitamin E-deficient and control animals, respectively. Cholinergic excitatory junction potentials were absent from 83 and 8% of vitamin E-deficient and control preparations, respectively. Responses to applied noradrenaline (0.1-30 microM), alpha,beta-methylene ATP (3-100 microM) and acetylcholine (0.1-30 microM) were attenuated or absent in vitamin E-deficient tissues. Responses to applied KCl were similar in both groups. Release of [3H]noradrenaline or endogenous acetylcholine could not be evoked from vitamin E-deficient tissues. 3. In contrast, in isolated preparations of the vas deferens and urinary bladder, neuromuscular transmission by adrenergic, cholinergic and purinergic components were unaffected by long-term vitamin E deficiency. 4. In conclusion, vitamin E deficiency causes dysfunction of autonomic neuroeffector mechanisms in the smooth muscle of the rat caecum, at both a pre- and postjunctional level. The lesions in autonomic transmission mechanisms brought about by long-term vitamin E deficiency were found only in the caecum; no changes in sympathetic neuromuscular transmission were observed in the vas deferens, or in parasympathetic neuromuscular transmission in the urinary bladder.
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PMID:Effects of vitamin E deficiency on autonomic neuroeffector mechanisms in the rat caecum, vas deferens and urinary bladder. 854 38

Diabetes mellitus often leads to generalized vasculopathy. Because of the pathophysiological role of free radicals we investigated the effects of vitamin E. Twenty-eight rats were rendered diabetic by streptozotocin injection and were fed either with a diet with low (10 mg/kg of chow), medium (75 mg/kg of chow) or high amounts of vitamin E (1300 mg/kg of chow). Nine age-matched nondiabetic rats receiving 75 mg of vitamin E/kg chow served as controls. After 7 months, mesenteric microcirculation was investigated. Smooth muscle contractile function was not altered in diabetic versus nondiabetic vessels. Endothelial function was significantly reduced in diabetics; relaxation upon 1 micro M acetylcholine was reduced by 50% in diabetics with a medium and high vitamin E diet. In vitamin E-deprived rats, a complete loss of endothelium-dependent relaxation was observed, and instead, acetylcholine elicited vasoconstriction. L-N(G)-Nitro-arginine-induced vasoconstriction was reduced in small arteries in diabetics, which was not prevented by vitamin E, but was aggravated by vitamin E deprivation. In a subchronic endothelial cell culture model, cells were cultivated with 5 or 20 mM D-glucose for an entire cell culture passage (4 days) with or without vitamin E (20 mg/l versus 0.01 mg/l). Hyperglycemia led to significant reduction in basal and ATP-stimulated nitric oxide (NO)-production. Hyperglycemia-induced reduction in basal NO-release was significantly prevented by vitamin E, whereas reduction in stimulated NO-release was not influenced. NADPH-diaphorase activity was reduced by 40% by hyperglycemia, which was completely prevented by vitamin E. We conclude that 1) vitamin E has a potential to prevent partially hyperglycemia-induced endothelial dysfunction, 2) under in vivo conditions vitamin E deficiency enhanced diabetic endothelial dysfunction dramatically, and 3) positive effects of vitamin E may be attenuated with a longer disease duration.
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PMID:Effect of chronic treatment with vitamin E on endothelial dysfunction in a type I in vivo diabetes mellitus model and in vitro. 1264 59