Gupta P, Kar A
Thyroid Research Unit, School of Life Sciences, Devi Ahilya University, Indore, India.
J Appl Toxicol. 1998 Sep-Oct;18(5):317-20. doi: 10.1002/(sici)1099-1263(1998090)18:5<317::aid-jat514>3.0.co;2-u.
A study on the effects of ascorbic acid (AA) on heavy metal (cadmium)-induced thyroid dysfunction and lipid peroxidation (LPO) was carried out in Swiss male mice. The animals were administered with either cadmium (1.0 mg kg(-1) body wt.) alone or in combination with AA (1 mM) every day for 15 days. While cadmium treatment led to a decrease in the serum concentrations of thyroid hormones and hepatic type I iodothyronine 5'-monodeiodinase (5'D-I) activity, an increase in the level of lipid peroxidation was observed. The metal-induced decrease in hepatic 5'D-I activity and serum triiodothyronine (T3) concentration was restored by treatment with AA. However, AA could not restore the serum thyroxine (T4) concentration. The increased level of LPO was also ameliorated by AA. It appears that the protective effect of AA against cadmium-induced thyroid dysfunction is mediated through its antioxidative action.
在瑞士雄性小鼠中开展了一项关于抗坏血酸（AA）对重金属（镉）诱导的甲状腺功能障碍和脂质过氧化（LPO）影响的研究。动物每天单独给予镉（1.0毫克/千克体重）或与AA（1毫摩尔）联合给药，持续15天。镉处理导致甲状腺激素血清浓度降低以及肝脏I型碘甲状腺原氨酸5'-单脱碘酶（5'D-I）活性下降，同时观察到脂质过氧化水平升高。用AA治疗可恢复金属诱导的肝脏5'D-I活性和血清三碘甲状腺原氨酸（T3）浓度降低。然而，AA不能恢复血清甲状腺素（T4）浓度。AA也改善了升高的LPO水平。看来，AA对镉诱导的甲状腺功能障碍的保护作用是通过其抗氧化作用介导的。
