| Summary: | 碩士 === 中原大學 === 化學研究所 === 96 === Our previous study indicated that electromagnetic field (EMF) treatment of mouse blastocysts induced apoptosis, decreased cell numbers, and retarded early postimplantation blastocyst development, in vitro. In this study, we further found that EMF treatment had cytotoxic effects on mouse blastocysts, and was associated with risk effects on their subsequent development, in vivo. Those result conformed to previous study entirely. Experiments also showed that 0.5 and 1.0 G EMF treatment induced various apoptotic biochemical changes including ROS generation, Bcl-2 expression level decrease, Bax expression level increase, loss of mitochondrial membrane potential, induction of cytochrome c release from the mitochondria to cytosol, and activation of caspase-9 and caspase-3. In addition, we also found that EMF treatment also caused caspase-8 activation in blastocysts. Furthermore, EMF-induced apoptosis was specifically blocked by a potent antioxidant, N-acetyl-cysteine (NAC), or caspases specific inhibitor, DEVD, LEHD and IETD. These results pointed out that EMF-induced apoptosis was ROS dependent and through the activation of caspases. Taken together, these results indicated that EMF treatment-induced apoptosis is via both mitochondria- and caspase-8-mediated apoptotic signal pathways, and caused embryonic development injury.
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