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本研究主要观察了睾酮对大鼠肝脏金属硫蛋白 (Metallothionein ,MT)诱导合成的作用 ,并动态观察了不同锌营养状态的大鼠在急性力竭运动后的恢复期中 ,肝脏金属硫蛋白诱导合成和锌、铜、铁离子含量的变化 ,探讨了它们之间的关系。结果显示 :大鼠皮下注射睾酮能够刺激诱导肝脏MT的合成。锌缺乏引起安静状态下大鼠肝脏MT含量下降 ,MT下降的原因可能与睾酮低下和锌离子减少有关。睾酮可能是MT在体内的正向调节因子。营养性锌缺乏不仅引起大鼠肝脏MT和锌基础水平的下降 ,而且导致急性力竭游泳后肝脏MT峰值较晚出现。这表明锌缺乏造成MT对运动的应激能力和合成速率下降 ,这将不利于运动后自由基的清除和组织的恢复。不管大鼠的锌营养状态如何 ,力竭游泳后 ,肝脏锌、铜、铁的含量均出现不同程度的升高或升高趋势。这些金属离子的升高和再分布 ,可能与MT的升高有关。
In this study, we observed the effect of testosterone on the induction of liver metallothionein (MT) synthesis in rats and dynamically observed the changes of liver metallothionein-induced synthesis in rats with different zinc nutrition during the recovery period after acute exhaustive exercise And zinc, copper, iron ion content changes, to explore the relationship between them. The results showed that subcutaneous injection of testosterone in rats could stimulate the synthesis of liver MT. The lack of zinc causes the MT content of rat liver to decrease in a quiet state. The reason for the decrease of MT may be related to the decrease of testosterone and the decrease of zinc ion. Testosterone may be a positive regulator of MT in the body. Nutritional zinc deficiency not only caused a decrease in basal levels of MT and zinc in rat liver, but also resulted in late appearance of liver MT peak after acute exhaustive swimming. This indicates that the lack of zinc causes the MT stress on the exercise capacity and the rate of synthesis decreased, which will not conducive to the removal of free radicals after exercise and tissue recovery. Regardless of the zinc nutritional status of rats, after exhaustive swimming, the contents of zinc, copper and iron in the liver all showed different degrees of increase or increase. The rise and redistribution of these metal ions may be related to the increase of MT.