Formaldehyde Exposure Induces Autophagy in Testicular Tissues of Adult Male Rats

Formaldehyde, a ubiquitous environmental pollutant, has long been suspected of causing adverse male reproductive effects. However, the molecular and cellular mechanisms underlying this phenomenon remain elusive. The overall aim of this study is to clarify the role of autophagy in male reproductive injuries induced by formaldehyde exposure, by which we can further understand the molecular mechanism of spermatogenesis and develop new targets for prevention and treatment of male infertility. In this study, electron microscopy, Western blot, and RT-PCR analysis were used to detect autophagy in testicular tissues. Moreover, testicular weights, histopathology, and morphometry were used to evaluate the reproductive injuries of formaldehyde exposure. We found that formaldehyde exposure-induced autophagy in testicular tissues was dose dependent. Increasing autophagosomes in spermatogenetic cells was observed by electron microscopy in formaldehyde exposure group. In addition, RT-PCR and Western blot analysis showed the transcription levels of the LC3-II, as well as the conversion from LC3-I to LC3-II, an indicator of autophagy, significantly increased in testicular tissue of formaldehyde exposure group in a dose dependent manner when compared with those in control group. Furthermore, the alterations of autophage were basically consistent with the changes in testicular weight and morphologic findings. In summary, formaldehyde exposure triggered autophagy, and autophagy may be a scathing factor responsible for male reproductive impairment induced by formaldehyde. (c) 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 323-331, 2015.

甲醛是一种普遍存在的环境污染物，长期以来被怀疑会对男性生殖产生不良影响。然而，这一现象背后的分子和细胞机制仍然不清楚。本研究的总体目标是阐明自噬在甲醛暴露诱导的男性生殖损伤中的作用，借此我们能够进一步了解精子发生的分子机制，并为男性不育的预防和治疗开发新的靶点。在本研究中，利用电子显微镜、蛋白质印迹法和逆转录聚合酶链反应分析来检测睾丸组织中的自噬情况。此外，通过睾丸重量、组织病理学和形态测量来评估甲醛暴露对生殖的损伤。我们发现甲醛暴露诱导的睾丸组织自噬具有剂量依赖性。在甲醛暴露组中，通过电子显微镜观察到生精细胞中的自噬体增多。此外，逆转录聚合酶链反应和蛋白质印迹法分析显示，与对照组相比，甲醛暴露组睾丸组织中自噬标志物LC3 - II的转录水平以及从LC3 - I到LC3 - II的转化显著增加，且呈剂量依赖性。此外，自噬的变化与睾丸重量和形态学结果的变化基本一致。总之，甲醛暴露引发自噬，自噬可能是导致甲醛诱导的男性生殖损伤的一个关键因素。（c）2013威利期刊公司。《环境毒理学》30：323 - 331，2015。