Effects of vitamin E on the platelet aggregation induced by combined adenosine diphosphate and hydrogen peroxide.

Polymorphisms in Catechol- O -Methyltransferase Modify Treatment Effects of Aspirin on Risk of Cardiovascular Disease

“…Recent data showing platelet COMT-mediated methylation-dependent inactivation of the common dietary antioxidant, quercetin 35 , may be indicative of a potential mechanism by which vitamin E effects may also depend on COMT genotype and activity. The COMT interaction with vitamin E is hypothesis generating, and may potentially offer some insight into the conflicting observations between animal and in-vitro studies 36 that support a role for vitamin E in minimizing cardiovascular risk, and overall null findings in CVD trials 19 . Thus, mechanistic studies that could account for this differential aspirin and vitamin E treatment effect by genotype are warranted, and may include analyses of platelet and vascular cell prostanoid and eicosanoid metabolism, oxidant stress, nitric oxide signaling, and platelet and endothelial function assessment over a wider range of doses.…”

Effects of riboflavin-2',3',4',5'-tetrabutyrate and flavin adenine dinucleotide on the platelet aggregation induced by hydrogen peroxide.

“…The platelet aggregation induced by H2O2 alone or in combination with ADP can be inhibited by vitamin E. It may be due to the antioxidant activity of vita min E, but it may also be partly due to the structural role for vitamin E in the membrane suggested by Lucy (Lucy 1972;Higashi and Ishigaki 1977). Thus it might be expected that FAD, and therefore its precursor, vitamin B2 derivative such as B2-BUT, can play a role to inhibit H2O2 induced platelet aggregation in concert with vitamin E.…”

“…The blood granulocytes could influence the platelet function via H2O2 generation (Canoso et al 1974; Levine et al 1976). H2O2 may either induce or inhibit or enhance the platelet aggregation depending upon the experi mental conditions (Higashi and Ishigaki 1977 …”