RESUMO
To investigate the role played by tamoxifen [TAM] as antioxidant as a part of the protective action of the drug against gamma irradiation. Forty female albino rats were used as the experimental animal model. Forty female rats were used riectomized and were divided into three subgroups of 5 animals each. The rats in two of these subgroups were treated with oral tamoxifen at a dose level of either 03 mg/kg/day or 0.6 mg/kg/day for 10 consecutive days. The third subgroup did not receive treatment and served as positive control. At the end of medication period all 15 animals received whole-body gamma irradiation dose of 6 Grays. Fifteen normal cyclic female rats were divided into the same subgroups, received similar treatment with tamoxifen and received the same irradiation dose as those in the ovariectomized group. Ten non-medicated non irradiated fen2ale rats served as negative control. The day following irradiation, animals were sacrificed and glutathione [GSR] was estimated in the blood. Livers were dissected and used for assays of GSH, thiobarbituric acid reactive substances, superoxide dismutase and glutathione peroxidase. Whole-body gamma irradiation of cyclic female rats with 6 Grays resulted in significant depletion of glutathione which was more prominent in the liver than in the blood. This was coupled with substantial increase in thiobarbituric acid reactive substances [TJ3ARS], representing lipid peroxidation products. Gamma irradiation also caused inhibition of the antioxidant enzymes superoxide dismutase [SOD] and glutathione peroxidase [GFx] Pretreatment with TAM [0.3 and 0.6 mg/kg]for 10 consecutive days suppressed the effect of i/radiation in a dosedependent manner. The effect of gamma-irradiation on ovariectomized rats was qualitatively the same as on cyclic animals. In ovariectomized animals the dose-dependence disappeared