Tapia G, Cornejo P, Fernández V, Videla L A
Programa de Farmacología Molecular y Clínica, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago.
Toxicol Lett. 1999 Jun 1;106(2-3):209-14. doi: 10.1016/s0378-4274(99)00068-5.
The influence of thyroid hormone administration (daily doses of 0.1 mg of 3,3',5-triiodothyranine (T3)/kg for 1-3 consecutive days) on rat liver protein oxidation was investigated in relation to the calorigenic and lipid peroxidative actions of the hormone. T3 treatment elicited a progressive enhancement in the serum levels of the hormone, the rectal temperature of the animals, and in the rate of O2 uptake of the liver, changes that are significantly correlated and evidence the development of thyroid calorigenesis. Liver lipid peroxidation was augmented by T3 administration as determined by the tissue content of thiobarbituric acid reactants, with a maximal effect (3.1-fold increase) being found at 2 days after treatment, whereas protein oxidation measured by the content of protein hydrazone derivatives exhibited a maximal 88% increase at 3 days. Maximal rates of lipid peroxidation occur at 1 day after the administration of T3, whereas those of protein oxidation are attained after treatment with three daily doses of T3, time at which the former levels off. It is concluded that T3 administration induces a substantial enhancement in hepatic protein oxidation, in addition to lipid peroxidation, that seems to be due to the higher oxidative stress status conditioned in the liver by thyroid calorigenesis. Both processes exhibit a differential time course of changes, that may represent differences in the susceptibility of target molecules to free radical attack and/or in the efficiency of repair mechanisms.
研究了连续1 - 3天每天给予大鼠0.1 mg 3,3',5 - 三碘甲状腺原氨酸（T3）/kg对大鼠肝脏蛋白质氧化的影响，并探讨了其与甲状腺激素产热及脂质过氧化作用的关系。T3处理使血清中甲状腺激素水平、动物直肠温度以及肝脏耗氧率逐渐升高，这些变化显著相关，表明甲状腺产热作用增强。通过硫代巴比妥酸反应物的组织含量测定发现，T3给药可增强肝脏脂质过氧化，在处理后2天达到最大效应（增加3.1倍），而通过蛋白质腙衍生物含量测定的蛋白质氧化在3天时最大增加88%。脂质过氧化的最大速率在给予T3后1天出现，而蛋白质氧化的最大速率在连续3天给予T3处理后达到，此时脂质过氧化速率趋于平稳。结论是，T3给药除了诱导脂质过氧化外，还能显著增强肝脏蛋白质氧化，这似乎是由于甲状腺产热作用使肝脏处于较高的氧化应激状态所致。这两个过程表现出不同的时间变化过程，这可能代表了靶分子对自由基攻击的敏感性差异和/或修复机制的效率差异。
