EFFECT OF VITAMIN-E ON HUMAN AORTIC ENDOTHELIAL-CELL RESPONSES TO OXIDATIVE INJURY

Reactive oxygen species produced by the cells present in the arterial wall may cause oxidative damage to cellular components altering endoth elial cell (EC) function. Changes in the EC function appear to play a key role in the pathogenesis of atherosclerosis. Human aortic endothel ial cells (HAEC) were employed to investigate the protective role of v itamin E upon exposure of endothelial cells to oxidative stress in vit ro. HAEC assimilate d-alpha-tocopherol from the media in a dose-depend ent manner. Exposure of HAEC to 16.5 mM of the free radical generator 2,2'-azobis (2-amidinopropane) hydrochloride (AAPH) for 16 h decreased cell viability (assessed by trypan blue exclusion) from 90 to 28%, HA EC preincubated with vitamin E at 15, 30, and 60 mu M prior to the AAP H exposure resulted in a dose-dependent increase in resistance to oxid ative stress and increased cell viability by 37, 66, and 85%, respecti vely, An increase in prostacyclin (PGI,) production by HAEC in respons e to AAPH exposure was correlated positively with cell damage and nega tively with vitamin E concentration. Interleukin (IL)-1 production als o increased in parallel with cell damage induced by AAPH. Vitamin E tr eatment significantly reduced IL-1 production after AAPH exposure, Thi s modulatory role of vitamin E on HAEC function following exposure to an oxidative stress may reflect its antioxidant protection against lip id peroxidation.