17 beta-estradiol protects against quinolinic acid-induced lipid peroxidation in the rat brain

The neurotoxin quinolinic acid has been identified as a causative agent in Huntington's disease and is a metabolite of the tryptophan pathway in the b rain. In the present study, the in vivo and in vitro effect of 17 beta -est radiol on lipid peroxidation induced by quinolinic acid was investigated. F or the in vivo experiments ovariectomized female rats were administered wit h 100 mug 17 beta -estradiol daily for seven days prior to and seven days f ollowing the intrahippocampal injection of 1 mu mol quinolinic acid. The le vel of lipid peroxidation in brain homogenate was investigated using the th iobarbituric acid test. The in vitro experiments were performed in brain ho mogenates of ovariectomized female rats. The homogenate was treated with qu inolinic acid alone or in combination with 17 beta -estradiol. Quinolinic a cid increased lipid peroxidation in a dose dependent manner in vitro, while homogenate co-treated with 17 beta -estradiol showed a significant reducti on in lipid peroxidation. 17 beta -estradiol was also shown to be protectiv e against quinolinic acid in vivo. These results could explain the neuropro tective effect of 17 beta -estradiol.