Increased oxidative stress is involved in the progression of many degenerative disease processes, including atherogenesis. Oxidative stress, combined with glycation, results in glycoxidative damage to matrix proteins. Current research indicates that estrogen is a potent antioxidant and has favorable effects on glucose tolerance and insulin levels. We undertook this study to examine the effects of 17-β estradiol (E2) on glycoxidative damage in the arterial wall. Two month-old ovariectomized rats were implanted for 6 months with hormone pellets containing either: 2.5mg E2; 25mg E2; 200mg progesterone(P4); 200mg P4+2.5mg E2; placebo or control(no pellet). Femoral arteries were removed and hydrolyzed. Pentosidine was then analyzed by HPLC. Pentosidine levels (in mmol pentosidine/mmol collagen) were markedly reduced in the 25mg E2, 2.5mg E2 and 2.5mg E2+P4-treated groups (7.8, 8.1 and 8.25, respectively) when compared to placebo (11.65), P4 (12.4) and control (13.4) groups. Estradiol-treated rats also tended (p = 0.08) to have decreased levels of plasma glucose (in mg/dL): 25mg E2 (94 ± 4), 2.5mg E2 (104 ± 9), 2.5mg E2 + P4 (114 ± 10), P4(122 ± 3), placebo (121 ± 5) and control(126 ± 11). We observed a similar trend (p = 0.08) in insulin levels between the treatment groups. In conclusion, E2 decreased glycoxidative damage in rat femoral arteries. This effect, at least in part, was due to decreased levels of circulating plasma glucose levels. Further studies are planned to examine the oxidative state of estrogen-treated arteries.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology