Amazoniac
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Legends of Kyrandia, a study done to explore the interaction of vits E and C
Partners in defense, vitamin E and vitamin C. - PubMed - NCBI
"To differentiate the role of cyclooxygenase and lipoxygenase in this AA-induced tocopherol oxidation, we conducted experiments in which platelet homogenates were preincubated with cyclooxygenase inhibitors prior to the addition of AA. Preincubation with known cyclooxygenase inhibitors such as aspirin or indomethacin markedly potentiated this AA-induced tocopherol oxidation."
"These results strongly support the hypothesis that AA-induced tocopherol oxidation in platelets is unrelated to cyclooxygenase but could be mediated by its 12-lipoxygenase activity."
Then they proceed to test different lipoxygenase products, and:
"To our great surprise, however, at 2.5 and 5 min after the addition of 12-HPETE, we detected the reappearance of tocopherol. These results reveal that when endogenous lipoxygenase is blocked by ETYA, 12-HPETE-induced oxidation of platelet tocopherol is reversible, suggesting the presence of endogenous reductant(s) that can be used to regenerate tocopherol."
The lords then added compounds that stopped the action of that other enzyme so that they could study the regeneration of tocopherol. Just like they did with aspirin.
After that, they added vit C and glutathione to compare their effects at the regeneration effects of tocopherol under the influence of AA.
"..the addition of ascorbate caused a rapid regeneration, which peaked at 1 min, by which time 64% of oxidized tocopherol was regenerated. In contrast: the addition of GSH caused a steady increase of the tocopherol level, which reached a maximum after 5 min."
"These findings illustrate the intricate dependency of membrane redox potential on cytosolic reductants
and further reinforce the notion that, in estimating the vitamin E requirement of man, other dietary factors such as ascorbate, selenium (a component of GSH peroxidase) , and unsaturated fatty acids should also be considered."
"Experimental evidence from animals and man has long established that polyunsaturated fat increases the requirement for vitamin E. Therefore, the turnover of membrane polyunsaturated fatty acids, a steady-state remodelling process of membrane phospholipids, may consume vitamin E via the lipoxygenase pathway. The rate of vitamin E consumption is expected to be much higher during inflammation, during which lipoxygenase activity and oxyradical production are much higher in inflammatory cells such as leukocytes and platelets. We have recently shown that oxidized vitamin E can also be regenerated in rat meutrophils (Ho and Chan 1992)."
Partners in defense, vitamin E and vitamin C. - PubMed - NCBI
"To differentiate the role of cyclooxygenase and lipoxygenase in this AA-induced tocopherol oxidation, we conducted experiments in which platelet homogenates were preincubated with cyclooxygenase inhibitors prior to the addition of AA. Preincubation with known cyclooxygenase inhibitors such as aspirin or indomethacin markedly potentiated this AA-induced tocopherol oxidation."
"Reduction of PGG2 to PGH2 has been shown to generate a tyrosyl radical, which inactivates cyclooxygenase, thereby limiting the amount of prostaglandins produced (Lassman et al. 1991)."
Which is why the compounds that inhibits the enzyme potentiate the tocopherol oxidation."These results strongly support the hypothesis that AA-induced tocopherol oxidation in platelets is unrelated to cyclooxygenase but could be mediated by its 12-lipoxygenase activity."
Then they proceed to test different lipoxygenase products, and:
"To our great surprise, however, at 2.5 and 5 min after the addition of 12-HPETE, we detected the reappearance of tocopherol. These results reveal that when endogenous lipoxygenase is blocked by ETYA, 12-HPETE-induced oxidation of platelet tocopherol is reversible, suggesting the presence of endogenous reductant(s) that can be used to regenerate tocopherol."
The lords then added compounds that stopped the action of that other enzyme so that they could study the regeneration of tocopherol. Just like they did with aspirin.
After that, they added vit C and glutathione to compare their effects at the regeneration effects of tocopherol under the influence of AA.
"..the addition of ascorbate caused a rapid regeneration, which peaked at 1 min, by which time 64% of oxidized tocopherol was regenerated. In contrast: the addition of GSH caused a steady increase of the tocopherol level, which reached a maximum after 5 min."
"These findings illustrate the intricate dependency of membrane redox potential on cytosolic reductants
and further reinforce the notion that, in estimating the vitamin E requirement of man, other dietary factors such as ascorbate, selenium (a component of GSH peroxidase) , and unsaturated fatty acids should also be considered."
"Experimental evidence from animals and man has long established that polyunsaturated fat increases the requirement for vitamin E. Therefore, the turnover of membrane polyunsaturated fatty acids, a steady-state remodelling process of membrane phospholipids, may consume vitamin E via the lipoxygenase pathway. The rate of vitamin E consumption is expected to be much higher during inflammation, during which lipoxygenase activity and oxyradical production are much higher in inflammatory cells such as leukocytes and platelets. We have recently shown that oxidized vitamin E can also be regenerated in rat meutrophils (Ho and Chan 1992)."