Low levels of alpha tocopherol(AT) ara related to atherosclerosis. In addition to decreasing LDL oxidation, AT may exert effects on cells crucial in atherogenesis, e.g., the monocyte(Mo). Hence, the aim of the present study was to test the effect of AT supplementation on Mo function, with regards to atherogenesi. Human blood Mo function was studied in 14 healthy volunteers at baseline, following 8 weeks(wk) of d-AT supplementation (1200IU/day) and following a 6-wk washout phase. The release of reactive oxygen speciea(ROS):hydrogen peroxide(H302) and Superoxide anion (02), and the oxidation of an artificial lipoprotein emulsion, consisting of cholesteryl linoleate, arachidonate, oleate and BSA was studied in the resting state and following activation of the monocytes with lipopolysaccharide(LPS). Lipid oxidation was measured by the TEARS(thiobarbituric acid reacting substances) assay. There was a 3-fold increase in AT levels when compared to baseline and washout phases. Release of ROS from Mo was decreased(4.) in resting and activated Mo following AT supplementation(H202: reating-50%A, p<0.002;activated-70%A, p<0.002. 02i resting70%4., p<0.003; activated-60%A, p<0.003). Lipid oxidation by activated Mo was significantly reduced at 8 wks(baeeline: 48.85120.38 vs. 8 wks: 28.44±9.46nmol/mg protein, p<0.002). Thus, alpha tocopherol supplementation moderates the oxidative tone of monocytea and may be a crucial therapy in atherosclerosis.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology