Chaurasia S S, Kar A
Thyroid Research Unit, School of Life Sciences, DA University, Indore, India.
Toxicology. 1997 Dec 31;124(3):203-9. doi: 10.1016/s0300-483x(97)00155-8.
The protective role of vitamin E (vit E) on lead-induced thyroid dysfunction with special reference to type-I iodothyronine 5'-monodeiodinase (5'D-I) activity in mice liver was investigated. Daily intraperitoneal (i.p.) injection of lead acetate (0.5 mg/kg body weight) for 30 days significantly decreased serum 3,3',5-triiodothyronine (T3) concentration and hepatic 5'D-I activity. Furthermore, lead significantly increased peroxidative reactions involving membrane components (lipid peroxidation, LPO) while the activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) were decreased in mouse liver. Simultaneous administration of vit E (5 mg/kg body weight) and 0.5 mg/kg body weight of lead restored thyroid function in mice by maintaining normal hepatic 5'D-I activity and serum thyroid hormone concentrations. It also prevented increase in LPO and inhibition of SOD and CAT activities in liver. We suggest that the intact membrane structure is a must for 5'D-I activity and the administration of vit E may prevent the lead induced thyroid dysfunction by maintaining membrane architecture.
研究了维生素E（vit E）对铅诱导的甲状腺功能障碍的保护作用，特别参考了小鼠肝脏中I型碘甲状腺原氨酸5'-单脱碘酶（5'D-I）的活性。每天腹腔注射醋酸铅（0.5毫克/千克体重），持续30天，显著降低了血清3,3',5-三碘甲状腺原氨酸（T3）浓度和肝脏5'D-I活性。此外，铅显著增加了涉及膜成分的过氧化反应（脂质过氧化，LPO），而小鼠肝脏中抗氧化酶如超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性降低。同时给予vit E（5毫克/千克体重）和0.5毫克/千克体重的铅，通过维持正常的肝脏5'D-I活性和血清甲状腺激素浓度，恢复了小鼠的甲状腺功能。它还防止了肝脏中LPO的增加以及SOD和CAT活性的抑制。我们认为完整的膜结构是5'D-I活性所必需的，vit E的给药可能通过维持膜结构来预防铅诱导的甲状腺功能障碍。
