Das K, Chainy G B
Biochemistry Unit, Department of Zoology, Utkal University, Bhubaneswar 751 004, India.
Biochim Biophys Acta. 2001 Jul 27;1537(1):1-13. doi: 10.1016/s0925-4439(01)00048-5.
In the present study the effect of thyroid hormone (T(3)) on oxidative stress parameters of mitochondria of rat liver is reported. Hypothyroidism is induced in male adult rats by giving 0.05% propylthiouracil (PTU) in drinking water for 30 days and in order to know the effect of thyroid hormone, PTU-treated rats were injected with 20 microg T(3)/100 g body weight/day for 3 days. The results of the present study indicate that administration of T(3) to hypothyroid (PTU-treated) rats resulted in significant augmentation of oxidative stress parameters such as thiobarbituric acid reactive substances and protein carbonyl content of mitochondria in comparison to its control and euthyroid rats. The hydrogen peroxide content of the mitochondria of liver increased in hypothyroid rats and was brought to a normal level by T(3) treatment. Induction of hypothyroidism by PTU treatment to rats also resulted in the augmentation of total and CN-sensitive superoxide dismutase (SOD) activities of the mitochondria, which was reduced when hypothyroid rats were challenged with T(3). Although CN-resistant SOD activity of the mitochondria remained unaltered in response to hypothyroidism induced by PTU treatment, its activity decreased when hypothyroid rats were injected with T(3). The catalase activity of the mitochondria decreased significantly by PTU treatment and was restored to normal when PTU-treated rats were given T(3). Total, Se-independent and Se-dependent glutathione peroxidase activities of the mitochondria were increased following PTU treatment and reduced when T(3) was administered to PTU-treated rats. The reduced and oxidised glutathione contents of the mitochondria of liver increased significantly in hypothyroid rats and their level was restored to normal when hypothyroid rats were injected with T(3). The results of the present study suggest that the mitochondrial antioxidant defence system is considerably influenced by the thyroid states of the body.
本研究报道了甲状腺激素（T(3)）对大鼠肝脏线粒体氧化应激参数的影响。通过在成年雄性大鼠饮用水中给予0.05%丙硫氧嘧啶（PTU）30天来诱导甲状腺功能减退，为了解甲状腺激素的作用，给经PTU处理的大鼠以20微克T(3)/100克体重/天的剂量注射3天。本研究结果表明，与对照和甲状腺功能正常的大鼠相比，给甲状腺功能减退（经PTU处理）的大鼠施用T(3)导致线粒体氧化应激参数如硫代巴比妥酸反应性物质和蛋白质羰基含量显著增加。甲状腺功能减退大鼠肝脏线粒体的过氧化氢含量增加，经T(3)处理后恢复到正常水平。用PTU处理大鼠诱导甲状腺功能减退也导致线粒体总超氧化物歧化酶（SOD）和对氰化物敏感的SOD活性增加，当用T(3)刺激甲状腺功能减退大鼠时，该活性降低。尽管线粒体对氰化物不敏感的SOD活性在PTU处理诱导的甲状腺功能减退反应中保持不变，但当给甲状腺功能减退大鼠注射T(3)时，其活性降低。PTU处理使线粒体的过氧化氢酶活性显著降低，给经PTU处理的大鼠施用T(3)后恢复正常。PTU处理后线粒体的总谷胱甘肽过氧化物酶、不依赖硒的谷胱甘肽过氧化物酶和依赖硒的谷胱甘肽过氧化物酶活性增加，给经PTU处理的大鼠施用T(3)时降低。甲状腺功能减退大鼠肝脏线粒体的还原型和氧化型谷胱甘肽含量显著增加，给甲状腺功能减退大鼠注射T(3)后其水平恢复正常。本研究结果表明，线粒体抗氧化防御系统受机体甲状腺状态的显著影响。
