Chaurasia S S, Gupta P, Kar A, Maiti P K
Environmental Physiology Laboratory, School of Life Sciences, Devi Ahilya University, Vigyan Bhawan, Indore, INDIA.
Biochem Mol Biol Int. 1996 Jul;39(4):765-70. doi: 10.1080/15216549600201851.
The possible involvement of lipid peroxidation (LPO) in the lead (Pb) and cadmium (Cd) induced thyroid dysfunction with special reference to type-I iodothyronine 5'-monodeiodinase (5'-D) activity was studied in rat liver homogenate. Peroxidative reactions involving membrane components were found to be markedly stimulated by chronic administration of Pb and Cd in rats. Metal induced inhibition in 5'-D activity was also observed. Since LPO is primarily an outcome of free radical generation, we suggest metal induced free radical mediated inhibition of 5'-D activity in rat liver homogenate. In addition, serum triiodothyronine (T3) and thyroxine (T4) concentrations were also decreased by metals.
在大鼠肝脏匀浆中研究了脂质过氧化（LPO）可能参与铅（Pb）和镉（Cd）诱导的甲状腺功能障碍，特别参考了I型碘甲状腺原氨酸5'-单脱碘酶（5'-D）的活性。发现涉及膜成分的过氧化反应在大鼠长期给予Pb和Cd后受到显著刺激。还观察到金属诱导的5'-D活性抑制。由于LPO主要是自由基产生的结果，我们认为金属诱导的自由基介导了大鼠肝脏匀浆中5'-D活性的抑制。此外，金属还降低了血清三碘甲状腺原氨酸（T3）和甲状腺素（T4）的浓度。
