Landry J, Chrétien P, de Muys J M, Morais R
Cancer Res. 1985 May;45(5):2240-7.
Normal and transformed chick embryo cells and their respective ethidium bromide-treated derivatives that are devoid of a functional respiratory chain were comparatively evaluated for their responses to hyperthermia treatment. No significant difference was found between the control and the respiration-deficient cells. The cells have a similar intrinsic thermosensitivity as judged by their capacity to form colonies after treatment at supraoptimal temperatures, and heat triggers in both cases an equal production of heat shock proteins and a strong induction of thermotolerance. In addition, sodium arsenite, carbonyl cyanide m-chlorophenylhydrazone, oligomycin, and antimycin A induce a similar heat shock protein response in the control and the treated cells. Based on these results, it is concluded that the inhibition by heat of the mitochondrial energy production does not constitute an obligatory rate-limiting event in hyperthermic cell killing and that the intracellular signal triggering development of thermotolerance or heat shock protein production does not obligatorily originate from damages to the respiratory chain. Moreover, the results indicate that the modifications responsible for the increased heat resistance of thermotolerant cells may not, or do not necessarily, involve a stabilization of the mitochondrial energy production.
对正常和转化的鸡胚细胞及其各自经溴化乙锭处理后缺乏功能性呼吸链的衍生物进行了比较，评估它们对高温处理的反应。在对照细胞和呼吸缺陷细胞之间未发现显著差异。从它们在超最适温度处理后形成集落的能力判断，这些细胞具有相似的内在热敏感性，并且在两种情况下，热都会引发等量的热休克蛋白产生和强烈的耐热性诱导。此外，亚砷酸钠、间氯苯腙羰基氰化物、寡霉素和抗霉素A在对照细胞和处理后的细胞中诱导相似的热休克蛋白反应。基于这些结果，可以得出结论：高温对线粒体能量产生的抑制在高温细胞杀伤中并非必然是限速事件，并且触发耐热性发展或热休克蛋白产生的细胞内信号不一定源于呼吸链的损伤。此外，结果表明，导致耐热细胞耐热性增加的修饰可能不涉及，或不一定涉及线粒体能量产生的稳定。
