Vitamin E suppresses bactericidal activity of polymorphonuclear leukocyte enhanced by hypoxia

Abstract

This investigation elucidates how various hypoxic interventions influence bactericidal activity of polymorphonuclear leukocyte (PMN) following treatment with an antioxidant vitamin E. Forty sedentary males were randomly assigned to vitamin E (n=20) and placebo (n=20) groups. Our results demonstrated that exposure to 12% O2 in the placebo group increased urinary 8‐isoprostane level and decreased plasma total antioxidant content. Moreover, this hypoxic exposure increased chemotactic, phagocytic, and oxidative burst activities of PMN, accompanied by increased expressions of L‐selectin, LFA‐1, Mac‐1, FcγIIIBR, C1qRp and C5aR on PMN. However, exposure to 12% O2 in the vitamin E group did not influence the opsonic/complement receptor expressions and bactericidal cascades of PMN. Additionally, the circulatory redox status, PMN‐mediated bactericidal activity and the opsonic/complement receptors on PMN were constant following exposure to 15%, 18% or 21% O2 in the two groups. We conclude that exposure to 12% O2 promotes PMN bactericidal activity, possibly by elevating lipid peroxidation. However, this hypoxic effect on PMN bactericidal activity is ameliorated by pretreatment with vitamin E.