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二噁英对精子发生的破坏:表观遗传重编程与易感性窗口期

Spermatogenesis disruption by dioxins: Epigenetic reprograming and windows of susceptibility.

作者信息

Pilsner J Richard, Parker Mikhail, Sergeyev Oleg, Suvorov Alexander

机构信息

Department of Environmental Health Sciences, University of Massachusetts Amherst, 686 N. Pleasant St., 171 Goessmann, Amherst, MA 01003-9303, USA.

Department of Genomics and Human Genetics, Vavilov Institute of General Genetics, Russian Academy of Sciences, 3 Gubkina St., 119991 Moscow, Russia; Chapaevsk Medical Association, 3a Meditsinskaya St., 446100 Chapaevsk, Samara Region, Russia.

出版信息

Reprod Toxicol. 2017 Apr;69:221-229. doi: 10.1016/j.reprotox.2017.03.002. Epub 2017 Mar 7.

DOI:10.1016/j.reprotox.2017.03.002
PMID:28286111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6143293/
Abstract

Dioxins are a group of highly persistent chemicals that are generated as by-products of industrial and natural processes. Reduction in sperm counts is among the most sensitive endpoints of dioxin toxicity. The exact mechanism by which dioxins reduce sperm counts is not known. Recent data implicate the role of epididymal factors rather than disruption of spermatogenesis. Studies reviewed here demonstrate that dioxins induce the transfer of environmental conditions to the next generation via male germline following exposures during the window of epigenetic reprogramming of primordial germ cells. Increased incidence of birth defects in offspring of male veterans exposed to dioxin containing, Agent Orange, suggest that dioxins may induce epigenomic changes in male germ cells of adults during spermatogenesis. This is supported by recent animal data that show that environmental conditions can cause epigenetic dysregulation in sperm in the context of specific windows of epigenetic reprogramming during spermatogenesis.

摘要

二噁英是一组具有高度持久性的化学物质,是工业和自然过程的副产品。精子数量减少是二噁英毒性最敏感的终点之一。二噁英降低精子数量的确切机制尚不清楚。最近的数据表明附睾因素的作用,而非精子发生的破坏。此处综述的研究表明,在原始生殖细胞表观遗传重编程窗口期暴露后,二噁英通过雄性生殖系将环境条件传递给下一代。接触含二噁英的橙剂的男性退伍军人后代出生缺陷发生率增加,表明二噁英可能在精子发生过程中诱导成年男性生殖细胞的表观基因组变化。最近的动物数据支持了这一点,这些数据表明环境条件可在精子发生过程中特定的表观遗传重编程窗口期导致精子表观遗传失调。

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