Transposable elements (TEs) comprise a group of repetitive sequences that bring positive, negative, as well as neutral effects to the host organism. Earlier considered as "junk DNA," TEs are now well-accepted driving forces of evolution and critical regulators of the expression of genetic information. Their activity is regulated by epigenetic mechanisms, including methylation of DNA and histone modifications. The loss of epigenetic control over TEs, exhibited as loss of DNA methylation and decondensation of the chromatin structure, may result in TEs reactivation, initiation of their insertional mutagenesis (retrotransposition) and has been reported in numerous human diseases, including cancer. Accumulating evidence suggests that these alterations are not the simple consequences of the disease, but often may drive the pathogenesis, as they can be detected early during disease development. Knowledge derived from the in vitro, in vivo, and epidemiological studies, clearly demonstrates that exposure to ubiquitous environmental stressors, many of which are carcinogens or suspected carcinogens, are capable of causing alterations in methylation and expression of TEs and initiate retrotransposition events. Evidence summarized in this review suggests that TEs are the sensitive endpoints for detection of effects caused by such environmental stressors, as ionizing radiation (terrestrial, space, and UV-radiation), air pollution (including particulate matter [PM]-derived and gaseous), persistent organic pollutants, and metals. Furthermore, the significance of these effects is characterized by their early appearance, persistence and presence in both, target organs and peripheral blood. Altogether, these findings suggest that TEs may potentially be introduced into safety and risk assessment and serve as biomarkers of exposure to environmental stressors. Furthermore, TEs also show significant potential to become invaluable surrogate biomarkers in clinic and possible targets for therapeutic modalities for disease treatment and prevention.

中文翻译：

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转座因子对环境压力的反应。


转座元件 (TE) 包含一组重复序列，可为宿主生物体带来积极、消极和中性的影响。 TE 早期被认为是“垃圾 DNA”，但现在已成为公认的进化驱动力和遗传信息表达的关键调节剂。它们的活性受到表观遗传机制的调节，包括 DNA 甲基化和组蛋白修饰。对 TE 的表观遗传控制的丧失，表现为 DNA 甲基化的丧失和染色质结构的去浓缩，可能会导致 TE 重新激活，启动插入突变（逆转录转座），并且已在包括癌症在内的许多人类疾病中得到报道。越来越多的证据表明，这些改变并不是疾病的简单后果，但往往可能驱动发病机制，因为它们可以在疾病发展的早期被检测到。来自体外、体内和流行病学研究的知识清楚地表明，暴露于普遍存在的环境应激源（其中许多是致癌物或疑似致癌物）能够引起甲基化和 TE 表达的改变并启动逆转录转座事件。本次综述中总结的证据表明，TE 是检测此类环境压力源影响的敏感终点，例如电离辐射（地面、太空和紫外线辐射）、空气污染（包括颗粒物 [PM] 衍生的和气态的） 、持久性有机污染物和金属。此外，这些效应的重要性在于其早期出现、持续性以及在靶器官和外周血液中的存在。 总而言之，这些发现表明 TE 有可能被引入安全和风险评估中，并作为暴露于环境压力源的生物标志物。此外，TE 还显示出成为临床上无价的替代生物标志物以及疾病治疗和预防的治疗方式的可能目标的巨大潜力。