Issels R D, Bourier S, Böning B, Li G C, Mak J J, Wilmanns W
Cancer Res. 1987 May 1;47(9):2268-74.
Chinese hamster ovary cells exposed to the sulfhydryl compound cysteamine combined with heat treatment at 44 degrees C developed thermotolerance within 8 h. After initial treatment either with 15 min cysteamine (0.4 mM) at 37 degrees C immediately followed by 15 min heat at 44 degrees C or with 15 min cysteamine (0.4 mM) at 44 degrees C, the magnitude of thermotolerance developed was identical. The D0 of the subsequent 44 degrees C heat survival curves increased by factors of 8.9 and 7.9, respectively. The kinetics of thermotolerance induction and the time to reach the maximum of thermotolerance expression after combined cysteamine treatment at 44 degrees C for 15 min was found to be comparable to the effects of 44 degrees C treatment alone for 30 min. The synergistic effect of cysteamine with the conditioning heat treatment at 44 degrees C was blocked by catalase (50 micrograms/ml). Following initial treatment with cysteamine at 37 degrees C, cells became thermotolerant within 2 h. The D0 of the survival curves for 44 degrees C heat treatments increased with duration (t1 = min, 37 degrees C) of the cysteamine (0.4 mM) exposure; e.g., the D0 increased by factors of 1.5, 1.6, 2.2, and 2.6 for t1 = 30, 60, 90, and 120 min. The induction of thermotolerance by cysteamine at 37 degrees C was completely blocked by the addition of catalase (50 micrograms/ml), present during the initial period of drug treatment. Combined cysteamine and heat treatment at 44 degrees C, but also cysteamine exposure at 37 degrees C, enhanced synthesis of heat shock proteins. The data suggest that oxidative stress by cysteamine can be synergistic with the conditioning heat treatment at 44 degrees C which induces thermotolerance. At 37 degrees C, cysteamine itself induces thermotolerance and the enhanced synthesis of heat shock proteins under these conditions.
将中国仓鼠卵巢细胞暴露于巯基化合物半胱胺并结合44℃的热处理，细胞在8小时内产生耐热性。在初始处理时，要么在37℃用15分钟的半胱胺（0.4 mM）处理，随后立即在44℃加热15分钟，要么在44℃用15分钟的半胱胺（0.4 mM）处理，所产生的耐热性程度是相同的。随后44℃热存活曲线的D0分别增加了8.9倍和7.9倍。发现在44℃用半胱胺处理15分钟后，耐热性诱导的动力学以及达到耐热性表达最大值的时间与单独用44℃处理30分钟的效果相当。半胱胺与44℃的预处理热处理的协同作用被过氧化氢酶（50微克/毫升）阻断。在37℃用半胱胺进行初始处理后，细胞在2小时内产生耐热性。44℃热处理存活曲线的D0随着半胱胺（0.4 mM）暴露时间（t1 =分钟，37℃）的延长而增加；例如，对于t1 = 30、60、90和120分钟，D0分别增加了1.5倍、1.6倍、2.2倍和2.6倍。在药物处理初期加入过氧化氢酶（50微克/毫升）可完全阻断37℃时半胱胺诱导的耐热性。44℃的半胱胺与热处理相结合，以及37℃的半胱胺暴露，均可增强热休克蛋白的合成。数据表明，半胱胺引起的氧化应激可与44℃的预处理热处理协同作用，从而诱导耐热性。在37℃时，半胱胺本身可诱导耐热性，并在这些条件下增强热休克蛋白的合成。
