Paula-Lopes F F, Hansen P J
Department of Animal Sciences, University of Florida, P.O. Box 110910, Gainesville, FL 32611-0910, USA.
Biochem Biophys Res Commun. 2002 Jul 5;295(1):37-42. doi: 10.1016/s0006-291x(02)00619-8.
Heat shock compromises development of preimplantation bovine embryos and the percentage of blastomeres labeled as TUNEL-positive. It was hypothesized that TUNEL labeling represents apoptosis and that apoptosis after heat shock is beneficial for continued embryonic development. To test these hypotheses, experiments were performed with z-DEVD-fmk, an inhibitor of group II caspases, on heat shock responses of embryos > or =16-cell stage at day 4 after insemination. Heat shock of 41 degrees C for 9 h increased group II caspase activity and the proportion of TUNEL positive cells; z-DEVD-fmk blocked these effects. The reduction in development of embryos exposed to heat shock for 6-9 h was magnified in the presence of z-DEVD-fmk. Results indicate that group II caspases mediate heat-induced apoptosis in bovine embryos and that inhibition of these caspases has a detrimental effect on embryonic resistance to heat shock. Apoptosis can be viewed as an adaptative mechanism to allow embryonic survival and development following stress.
热休克会损害植入前牛胚胎的发育以及标记为TUNEL阳性的卵裂球百分比。据推测，TUNEL标记代表细胞凋亡，热休克后的细胞凋亡有利于胚胎的持续发育。为了验证这些假设，使用II型半胱天冬酶抑制剂z-DEVD-fmk对授精后第4天≥16细胞期的胚胎热休克反应进行了实验。41℃热休克9小时会增加II型半胱天冬酶活性和TUNEL阳性细胞比例；z-DEVD-fmk可阻断这些效应。在z-DEVD-fmk存在的情况下，暴露于热休克6 - 9小时的胚胎发育减少情况会加剧。结果表明，II型半胱天冬酶介导牛胚胎热诱导的细胞凋亡，抑制这些半胱天冬酶对胚胎耐热休克能力有不利影响。细胞凋亡可被视为一种适应性机制，以允许胚胎在应激后存活和发育。
