Heat shock but not cold shock leads to disturbed intracellular zinc homeostasis

Abstract

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.

Optimization of a Methodology for Quantification and Removal of Zinc Gives Insights Into the Effect of This Metal on the Stability and Function of the Zinc-Binding Co-chaperone Ydj1

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Physiological factors could enhance amyloid-beta toxicity

“…During heat (or other environmental) stress response Zn 2+ ions are released from metallothioneins (Pirev et al, 2010), resulting the increase of intracellular Zn 2+ concentration. Moreover, depolarization during neurotransmission or evoked artificially by electric stimulation (Howell et al, 1984, Aniksztejn et al, 1987, by administration of K + (Assaf and Chung, 1984, Charton et al, 1985, Aniksztejn et al, 1987 or by kainic acid (Assaf andChung, 1984, Charton et al, 1985) cause the release of Zn 2+ from hippocampal neuronal terminals into the synaptic cleft (Aniksztejn et al, 1987), thus extracellular Zn 2+ concentration raises.…”