فایل آنتی اکسیدان ۶ ( Anti oxidant )

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فایل آنتی اکسیدان ۶ ( Anti oxidant )

چکیده:

Antioxidant Protection of LDL by Physiological Concentrations of 17ß-Estradiol

Background Exposure to estrogens reduces the risk for coronary artery disease and associated clinical events; however, the mechanisms responsible for these observations are not clear. Supraphysiological levels of estrogens act as antioxidants in vitro, limiting oxidation of low-density lipoprotein (LDL), an event implicated in atherogenesis. We investigated the conditions under which physiological concentrations of 17ß-estradiol (E_۲) inhibit oxidative modification of LDL. Methods and Results Plasma incubated with E_۲ (۰.۱ to 100 nmol/L) for 4 hours yielded LDL that demonstrated a dose-related increase in resistance to oxidation by Cu^۲+ as measured by conjugated diene formation. This effect was dependent on plasma, because incubation of isolated LDL with E_۲ at these concentrations in buffered saline produced no effect on Cu^۲+-mediated oxidation. Incubation of plasma with E_۲ had no effect on LDL -tocopherol content or cholesteryl ester hydroperoxide formation during the 4-hour incubation. Plasma incubation with [^۳H]E_۲ was associated with dose-dependent association of ^۳H with LDL. High-performance liquid chromatographic analysis of LDL derived from plasma incubated with [^۳H]E_۲ indicated that the majority of the associated species were not detectable as authentic E_۲ but as nonpolar forms of E_۲ that were susceptible to base hydrolysis consistent with fatty acid esterification of E_۲. Plasma-mediated association of E_۲ and subsequent antioxidant protection was inhibited by 5,5″-dithio-bis(2-nitrobenzoic acid), an inhibitor of plasma acyltransferase activity. Conclusions Exposure of LDL to physiological levels of E_۲ in a plasma milieu is associated with enhanced resistance to Cu^۲+-mediated oxidation and incorporation of E_۲ derivatives into LDL. This antioxidant capacity may be another means by which E_۲ limits coronary artery disease in women.