Institute of Biochemistry and Molecular Biology I, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
J Cell Physiol. 2010 Apr;223(1):103-9. doi: 10.1002/jcp.22016.
The heat shock response is a highly conserved process essential for surviving environmental stress, including extremes of temperature. To investigate whether heat shock has an impact on intracellular Zn(2+) homeostasis, cells were subjected to heat shock, and subsequently the intracellular free zinc concentration was investigated. Sublethal heat shock induced a temperature-dependent and transient intracellular Zn(2+) release that was repeatable after 24 h. The free zinc was localized in round-shaped nuclear bodies identified as nucleoli. Metallothionein, the main cellular zinc storing protein, was found to be not functionally essential for this heat-shock-induced effect. No significant oxidative stress within the cells was detected after heat shock. Cold shock and subsequent rewarming did not result in disturbed intracellular zinc homeostasis. These results show that heat shock and cold shock differ with respect to intracellular Zn(2+) release. A role for zinc as signaling ion during fever is conceivable.
热休克反应是一种高度保守的过程，对于在包括极端温度在内的环境压力下生存至关重要。为了研究热休克是否对细胞内 Zn(2+)稳态有影响，将细胞进行热休克处理，随后研究细胞内游离锌浓度。亚致死性热休克诱导了一种与温度相关的、短暂的细胞内 Zn(2+)释放，24 小时后可重复发生。游离锌定位于被鉴定为核仁的圆形核体内。金属硫蛋白，主要的细胞内锌储存蛋白，对于这种热休克诱导的效应并非必需。热休克后，细胞内没有检测到明显的氧化应激。冷休克和随后的复温也没有导致细胞内锌稳态紊乱。这些结果表明，热休克和冷休克在细胞内 Zn(2+)释放方面存在差异。锌作为发热期间的信号离子的作用是可以想象的。
