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Male-mediated developmental toxicity

机译:男性介导的发育毒性

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摘要

Male-mediated developmental toxicity has been of concern for many years. The public became aware of male-mediated developmental toxicity in the early 1990s when it was reported that men working at Sellafield might be causing leukemia in their children. Human and animal studies have contributed to our current understanding of male-mediated effects. Animal studies in the 1980s and 1990s suggested that genetic damage after radiation and chemical exposure might be transmitted to offspring. With the increasing understanding that there is histone retention and modification, protamine incorporation into the chromatin and DNA methylation in mature sperm and that spermatozoal RNA transcripts can play important roles in the epigenetic state of sperm, heritable studies began to be viewed differently. Recent reports using molecular approaches have demonstrated that DNA damage can be transmitted to babies from smoking fathers, and expanded simple tandem repeats minisatellite mutations were found in the germline of fathers who were exposed to radiation from the Chernobyl nuclear power plant disaster. In epidemiological studies, it is possible to clarify whether damage is transmitted to the sons after exposure of the fathers. Paternally transmitted damage to the offspring is now recognized as a complex issue with genetic as well as epigenetic components.
机译:雄性介导的发育毒性多年来一直受到关注。在1990年代初,当人们报道在塞拉菲尔德工作的男性可能在其子女中引起白血病时,公众开始意识到男性介导的发育毒性。人类和动物研究为我们目前对男性介导作用的理解做出了贡献。 1980年代和1990年代的动物研究表明,辐射和化学暴露后的遗传损害可能会传播给后代。随着人们对组蛋白的保留和修饰,鱼精蛋白掺入成熟精子的染色质和DNA甲基化以及精子的RNA转录物在精子的表观遗传状态中起重要作用的认识日益加深,可遗传的研究开始出现不同的看法。最近使用分子方法的报告表明,DNA损伤可以从吸烟父亲那里传播给婴儿,并且在暴露于切尔诺贝利核电站灾难辐射的父亲的种系中发现了扩展的简单串联重复小卫星突变。在流行病学研究中,可以弄清楚在父亲接触后是否将损害传给儿子。父系传播对后代的损害现已被认为是遗传和表观遗传成分的复杂问题。

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