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gamma tocopherol/versterkte bloedingsneiging

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Increased levels of F2-isoprostanes following aneurysmal subarachnoid hemorrhage in humans.

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Subarachnoid hemorrhage (SAH) resulting from aneurysmal rupture is the major cause of nontraumatic SAH. We hypothesized that oxidative stress could be increased following aneurysmal SAH due to hemoglobin release and ischemia-reperfusion injury and that may further contribute to poor outcome. We
Antioxidants occasionally have become prooxidants when a large amount was ingested. The haemorrhagic toxicity of butylated hydroxytoluene, a synthetic antioxidant, may involve such a mechanism. This study investigated whether haemorrhage is induced by overdoses of tocopherols, beta-carotene,

Relation of serum α- and γ-tocopherol levels to cardiovascular disease-related mortality among Japanese men and women.

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BACKGROUND There is limited evidence regarding the relationship between serum tocopherol levels and cardiovascular disease. METHODS We conducted a nested case-control study as part of the Japan Collaborative Cohort Study for evaluation of cancer risk (JACC Study). Baseline serum samples were

Oxidative stress resulting from hemolysis and formation of catalytically active hemoglobin: protective strategies.

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OBJECTIVE The possible oxidative complications induced by free hemoglobin (Hb) released during the blood storage are discussed together with therapeutic strategies using vitamin E and specific inhibitor haptoglobin. Prooxidative properties of Hb in blood have been examined using LDL as a marker for

Serum tocopherol levels in very preterm infants after a single dose of vitamin E at birth.

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OBJECTIVE Our aim was to examine the impact of a single enteral dose of vitamin E on serum tocopherol levels. The study was undertaken to see whether a single dose of vitamin E soon after birth can rapidly increase the low α-tocopherol levels seen in very preterm infants. If so, this intervention

Vitamin E Status and Neurodegenerative Disease.

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Vitamin E (alpha-and gamma-tocopherol) may slow the progression of a number of major degenerative diseases of the nervous system that appear to be significantly worsened by oxidative stress. The effects of vitamin E on excitoxicity in cultured neurones is considered, together with ataxia due to
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