Inhibition by oestradiol of oxidative stress-induced apoptosis in pig ovarian tissues.

Oxidative stress-induced apoptotic cell death has been implicated in the mechanisms of corpus luteum regression and follicular atresia. The objective of this investigation was to determine whether the antioxidant, oestradiol influenced apoptosis in pig luteal and follicular tissues exposed in vitro to hydrogen peroxide. Immunolocalization of fragmented DNA (a biochemical marker of apoptosis) in large steroidogenic luteal and granulosa cells was inhibited by oestradiol. Protection against apoptosis required relatively high concentrations of oestradiol (> or = 40 pg ml-1 incubation media) and was largely unmitigated by actinomycin D (suggesting a predominantly receptor-independent nongenomic mode of action). Ovarian cells were not protected by other (nonaromatizable) steroid hormones. It is suggested that oestradiol functions at the ovary as a reactive oxygen scavenger during pregnancy-mediated luteal rescue and folliculogenesis.