SHORT TERM VITAMIN E SUPPLEMENTATION HAS NO EFFECT ON PLATELET FUNCTION, PLASMA PHOSPHOLIPASE A₂ AND LYSO‐PAF IN MALE VOLUNTEERS

Abstract

1. Based largely upon in vitro studies, vitamin E has been reported to inhibit phospholipase A2 activity, to alter phospholipid metabolism and reduce platelet aggregation. 2. The effect of dietary supplementation with D-alpha-tocopherol (1500 iu/day for 14 days) was studied in nine males, 41-63 years old, comparing active treatment with a preceding placebo period. 3. Despite an increase from 2.6 +/- 0.8 (s.d.) x 10(-5) mol/L to 6.0 +/- 1.8 10(-5) mol/L in plasma vitamin E there were no significant changes in the aggregation of diluted whole blood or platelet rich plasma to adenosine diphosphate (ADP) or collagen, in plasma phospholipase A2 activity or plasma lyso-platelet-activating factor (lyso-PAF) (bioassay after in vitro acetylation to PAF). 4. High dose vitamin E dietary supplementation had no effect on these phospholipid and platelet parameters.

Gemfibrozil‐induced decrease in serum ubiquinone and α‐ and γ‐tocopherol levels in men with combined hyperlipidaemia

“…Indeed, platelets exposed to minimally oxidized LDL in vitro aggregate easily [40,41]. Moreover, vitamin E supplementation of healthy volunteers attenuates platelet activity in vitro and in vivo [42], although conflicting results have been reported [43]. In the present study, the gemfibrozil-induced reduction of serum antioxidants was paralleled by platelet activation in vivo, as evidenced by enhanced platelet aggregation and an increase in the urinary excretion of the platelet-specific product 11dehydro-thromboxane B 2 [21].…”

A metabolomic investigation of the effects of vitamin E supplementation in humans

“…Vitamin E has been shown to influence gene expression of a number of systems and modulate the activities of a number of enzymes involved in signal transduction, including PLA 2 [41]. Depending on the model used vitamin E treatment has been shown to activate [37,42,43], inhibit [44-46] or have no effect [47] on PLA 2 activity, but the weight of evidence overall is suggestive of an increase in PLA 2 activity following vitamin E exposure in cell/animal models. Because of the difference in models used and lack of human data it is not possible to relate PLA 2 activity with vitamin E levels.…”

Short-term, Moderate Dosage Vitamin E Supplementation May Have No Effect on Platelet Aggregation, Coagulation Profile, and Bleeding Time in Healthy Individuals

“…No change in aggregation of the Vitamin E groups was noted to epinephrine or ADP [28]. Silbert et al in 1990 proved no effect on aggregation using 1500 IU/day of natural ␣-tocopherol and whole blood [27]. Further, Liu et al showed inhibited aggregation to 8 weeks of mixed tocopherols (␥, ␦, ␣) when stimulated by PMA, but not to ␣-tocopherol alone when stimulated by ADP and PMA [35].…”

“…There have been isolated reports of adverse reactions to Vitamin E such as headache, fatigue, nausea, diplopia, muscular weakness and gastrointestinal distress at doses Ͼ1000 IU per day for prolonged periods. However, several studies have verified the safety and excellent tolerability of the supplement in doses Ͼ1000 IU per day [17,18,[26][27][28]. Steiner and Anastasi reported an in vivo study with four patients using escalating doses of dl-␣-tocopherol acetate from 600 to 2400 IU/day at 1 week intervals.…”

“…The preponderance of the in vivo and in vitro human and animal data suggest an inhibitory effect on platelet aggregation and adhesion at various concentrations of Vitamin E [1, 16 -24, 29 -34, 36 -37]; however, multiple human studies have refuted this anti-platelet aggregation theory [25][26][27][28]35]. Tables 2 and 3 review a selection of in vitro and in vivo studies related to Vitamin E and platelet aggregation.…”