热休克诱导小白鼠心、肝、肾、肺、脑等组织细胞SOD活性非常显著或显著升高,其中主要诱导CuZn-SOD的生物合成;42℃诱导小白鼠各组织细胞CAT活性极显著下降,正常情况下,脑细胞几乎不存在CAT活性,42℃热休克20min诱导脑CAT活力升高;热休克亦诱导各组织cSH-Px活性变化,心、脑细胞GSH-Px极显著升高,对肺的影响较小。SOD、CAT、GSH-Px协同作用,维持机体正常生理机能。还探讨了热休克应答、热耐受能力的获得与抗氧化酶活性变化存在的对应关系。 Heat shock induced SOD activity in heart, liver, kidney, lung, brain and other tissues of mice was very significantly or significantly increased, which mainly induced the biosynthesis of CuZn-SOD; the CAT activity of the cells induced by 42 ℃ decreased significantly, Under normal conditions, there is almost no activity of CAT in brain cells. Heat shock at 42 ℃ for 20 min induces an increase in CAT activity. Heat shock also induces changes in cSH-Px activity in each tissue. GSH-Px in heart and brain cells is significantly increased. Less affected. SOD, CAT, GSH-Px synergies to maintain the body’s normal physiological function. Also discussed the heat shock response, access to heat tolerance and changes in antioxidant enzyme activity exist correspondence.