以體外培養與動物實驗探討電磁場對小鼠胚胎發育之傷害

先前體外實驗的研究結果指出電磁場會引起小鼠囊胚細胞的凋亡，減少細胞數目，並且阻礙後續胚胎的發育。本論文研究進一步以動物實驗發現電磁場會引起小鼠囊胚細胞的凋亡和降低細胞增生，並且影響胚胎後續的發育，此發現與先前以體外培養的研究的結果互相符合。實驗亦證明，以 0.5 及 1.0 高斯電磁場刺激會引起囊胚細胞中許多凋亡訊息的改變，包含氧化壓力 (ROS) 的產生，Bcl-2 表現量減少，Bax表現量增加，粒線體膜電位降低，並且使細胞色素C (cytochrome c) 由粒線體釋放至細胞質，接著引發 caspase 9 與 caspase 3 的活化。除此之外，也發現caspase 8 有活化的情形。進一步證實電磁場引發的凋亡能有效受到抗氧化劑 N-acetyl-cysteine (NAC) 的阻斷以及caspases 專一性抑制劑的抑制。因此推測以電磁場刺激後，透過氧化壓力的產生，造成 caspase 3、caspase 9 及capase 8活化，進而引發囊胚細胞凋亡。綜合以上實驗的結果，明確指出電磁場引發小鼠囊胚細胞凋亡是透過粒線體和 caspase-8 所參與的兩條不同的凋亡訊息傳遞路徑而來，進而傷害小鼠胚胎的發育。

關鍵字

細胞凋亡；胚胎；囊胚；電磁場

並列摘要

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.

並列關鍵字

apoptosis ； electromagnetic field ； blastocyst ； embryo

參考文獻

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以體外培養與動物實驗探討電磁場對小鼠胚胎發育之傷害

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