Stohs S J, Hassan M Q, Murray W J
Xenobiotica. 1984 Jul;14(7):533-7. doi: 10.3109/00498258409151443.
Daily treatment of female rats with butylated hydroxyanisole (BHA) protected against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) toxicity. This protective effect was associated with reduced microsomal lipid peroxidation, increased glutathione peroxidase (GSH-PX) activity and decreased aryl hydrocarbon hydroxylase (AHH) activity. Retinol acetate (vitamin A) inhibited lipid peroxidation, elevated GSH-PX activity, and enhanced AHH activity. Thirty per cent of vitamin A-treated animals were alive 25 d after a lethal dose of TCDD. d-alpha-Tocopherol (vitamin E) inhibited markedly microsomal lipid peroxidation, enhanced AHH activity, and had no effect on GSH-PX activity. Only 10% of the vitamin E-treated animals were alive 25 d after a lethal dose of TCDD. The mechanism of TCDD toxicity may involve in part inhibition of GSH-PX activity with resultant lipid peroxidation by hydrogen peroxide.
用丁基羟基茴香醚（BHA）每日处理雌性大鼠可预防2,3,7,8-四氯二苯并对二恶英（TCDD）的毒性。这种保护作用与微粒体脂质过氧化作用降低、谷胱甘肽过氧化物酶（GSH-PX）活性增加以及芳烃羟化酶（AHH）活性降低有关。醋酸视黄醇（维生素A）可抑制脂质过氧化作用，提高GSH-PX活性，并增强AHH活性。30%经维生素A处理的动物在给予致死剂量的TCDD后25天仍存活。d-α-生育酚（维生素E）可显著抑制微粒体脂质过氧化作用，增强AHH活性，而对GSH-PX活性无影响。仅10%经维生素E处理的动物在给予致死剂量的TCDD后25天仍存活。TCDD毒性的机制可能部分涉及GSH-PX活性的抑制以及由此导致的过氧化氢引发的脂质过氧化作用。
