【摘要】 本研究动态观察了急性力竭游泳后不同锌营养状态的大鼠肝脏金属硫蛋白 (Metallothionein,MT)诱导合成和锌、铜、铁离子含量的变化 ,分析了它们之间的关系。结果显示 :营养性锌缺乏引起安静状态下大鼠肝脏 MT和锌含量的下降。缺锌大鼠补锌后 ,肝脏 MT和锌含量均明显回升。这表明 MT的合成与锌营养状况有关。锌营养正常的大鼠急性力竭游泳后 ,肝脏 MT含量升高 ,6 h达高峰 ,随后下降。 MT的升高与运动恢复期中金属离子代谢增强和自由基清除有关。锌缺乏大鼠急性力竭游泳后 ,肝脏 MT的峰值出现得又晚又低 ,表明锌缺乏影响了 MT对运动的应激水平和诱导合成速率 ,这将不利于运动后的恢复。锌缺乏引起肝脏铁含量的明显升高 ,升高的铁离子有可能造成氧化损伤。 MT基础水平的下降和应激诱导能力的减弱 ,以及锌、铁离子代谢的紊乱 ,可能是营养性锌缺乏影响运动能力的原因之一。更多还原

【Abstract】 The effects of different zinc nutritional status on the induction of metallothionein (MT) and the content changes of zinc, copper, and iron in rat liver after acute exhaustive swimming were observed. The relationship between MT and the metal ions were also analyzed. The results showed that the concentrations of MT and zinc in liver of zinc deficiency rats were reduced, and then returned back after zinc replenishment, indicating that the induction and synthesis of MT is dependent on zinc status. It was demonstrated that liver MT rose and reached to the peak at 6h after acute exhaustive swimming in rats with normal zinc status. The increase of liver MT was supposed to associate with the active metal mineral metabolism and the scavenging of free radicals during recovery period. Compared with normal rats, acute exhaustive swimming induced peak value of liver MT in zinc deficient rats appeared later and in a lower level, which shows clearly that the potential and induction of hepatic MT in stress is affected by zinc deficiency, implying an unfavorable situation to post exercise recovery. Zinc deficiency led to higher liver iron concentration that would result in oxidative stress and tissue damage. It is suggested that decreased basal MT level and reduced MT induction potential in stress, as well as the deranged zinc and iron metabolisms under zinc deficient condition would be one of the mechanisms by which the exercise capacity is harmed by zinc deprivation.更多还原