Exposure to bisphenol A (BPA) has been related to male reproductive disorders. Since this endocrine disruptor also displays genotoxic and epigenotoxic effects, it likely alters the spermatogenesis, a process in which both hormones and chromatin remodeling play crucial roles. The hypothesis of this work is that BPA impairs early embryo development by modifying the spermatic genetic and epigenetic information. Zebrafish males were exposed to 100 and 2000 μg/L BPA during early spermatogenesis and during the whole process. Genotoxic and epigenotoxic effects on spermatozoa (comet assay and immunocytochemistry) as well as progeny development (mortality, DNA repairing activity, apoptosis and epigenetic profile) were evaluated. Exposure to 100 µg/L BPA during mitosis slightly increased sperm chromatin fragmentation, enhancing DNA repairing activity in embryos. The rest of treatments promoted high levels of sperm DNA damage, triggering apoptosis in early embryo and severely impairing survival. Regarding epigenetics, histone acetylation (H3K9Ac and H3K27Ac) was similarly enhanced in spermatozoa and embryos from males exposed to all the treatments. Therefore, BPA male exposure jeopardizes embryonic survival and development due to the transmission of a paternal damaged genome and of a hyper-acetylated histone profile, both alterations depending on the dose of the toxicant and the temporal window of exposure.

译文

:双酚A(BPA)的暴露与男性生殖系统疾病有关。由于这种内分泌干扰物还具有遗传毒性和表观遗传毒性作用,因此它很可能改变了精子发生过程,在此过程中激素和染色质的重塑都起着至关重要的作用。这项工作的假设是,双酚A通过修饰精子遗传和表观遗传信息来损害早期胚胎发育。斑马鱼的雄性在早期生精过程中和整个过程中都暴露于100和2000μg/ L BPA。评估了对精子的遗传毒性和表观遗传毒性作用(彗星试验和免疫细胞化学)以及子代发育(死亡率,DNA修复活性,细胞凋亡和表观遗传特征)。有丝分裂期间暴露于100μg/ L BPA会稍微增加精子染色质的碎片,从而增强胚胎中的DNA修复活性。其余的治疗促进了高水平的精子DNA损伤,触发了早期胚胎中的细胞凋亡,并严重损害了存活率。关于表观遗传学,在接受所有治疗的雄性精子和胚胎中,组蛋白乙酰化(H3K9Ac和H3K27Ac)同样得到增强。因此,由于父本受损基因组和高乙酰化组蛋白谱的传递,BPA男性暴露危害胚胎存活和发育,这两种改变均取决于毒物的剂量和暴露的时间窗。

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