Kapron-Brás C M, Hales B F
Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
Teratology. 1992 Aug;46(2):191-200. doi: 10.1002/tera.1420460212.
Heat-induced cross-tolerance to cadmium was investigated in two inbred strains of mice, BALB/c and SWV, using a whole embryo culture system. Embryos were exposed to a pretreatment of 5 min at 43 degrees C and subsequently to an embryotoxic concentration of cadmium, 1.75 microM. The two types of embryos responded differently to the heat pretreatment, as cross-tolerance was induced in SWV but not in BALB/c mice. In SWV embryos, prior exposure to 43 degrees C for 5 min essentially eliminated the negative effects of cadmium on embryonic development and growth. However, in BALB/c embryos, no protection was observed. The variation in development of cross-tolerance in embryos from the two strains of mice was not correlated with differences in the induction of a 68-kD heat-shock protein (hsp68). There was a rapid increase in this protein in both strains after the initial heat exposure but not excess induction in the SWV strain that developed tolerance. The induction of hsp68 is therefore not sufficient to elicit cross-tolerance, and other mechanisms are likely to be important in the protective response of the embryo.
利用全胚胎培养系统，在两种近交系小鼠BALB/c和SWV中研究了热诱导的对镉的交叉耐受性。胚胎先在43℃下预处理5分钟，随后暴露于胚胎毒性浓度的镉（1.75微摩尔）中。两种胚胎对热预处理的反应不同，因为SWV小鼠诱导出了交叉耐受性，而BALB/c小鼠没有。在SWV胚胎中，预先在43℃下暴露5分钟基本消除了镉对胚胎发育和生长的负面影响。然而，在BALB/c胚胎中，未观察到保护作用。两种品系小鼠胚胎交叉耐受性发育的差异与68-kD热休克蛋白（hsp68）诱导的差异无关。初次热暴露后，两种品系中该蛋白均迅速增加，但在产生耐受性的SWV品系中没有过度诱导。因此，hsp68的诱导不足以引发交叉耐受性，其他机制可能在胚胎的保护反应中起重要作用。
