Gestational exposure to low‐dose zearalenone disrupting offspring spermatogenesis might be through epigenetic modifications. Issue 4 (29th May 2019)

• Record Type: Journal Article
• Authors: Men, Yuhao; Zhao, Yong; Zhang, Pengfei; Zhang, Hongfu; Gao, Yishan; Liu, Jing; Feng, Yanni; Li, Lan; Shen, Wei; Sun, Zhongyi; Min, Lingjiang
• Is Part Of: Basic & clinical pharmacology & toxicology. Volume 125:Issue 4(2019)
• Page Start: 382
• Page End: 393
• Publication Date: 2019-05-29
• Subjects: disrupting -- epigenetic pathways -- gestational exposure -- offspring -- spermatogenesis -- zearalenone; Pharmacology -- Periodicals; Toxicology -- Periodicals; Pharmacology -- Periodicals; Toxicology -- Periodicals; Pharmacology, Clinical -- Periodicals; Computer network resources; Electronic journals; 615.1
• DOI: 10.1111/bcpt.13243
• Languages: English
• ISSNs: 1742-7835

Abstract

Abstract: Zearalenone (ZEA), a F‐2 mycotoxin produced by Fusarium, has been found to be an endocrine disruptor through oestrogen receptor signalling pathway to impair spermatogenesis. The disruption on reproductive systems by ZEA exposure might be transgenerational. In our previous report, we have found that low dose (lower than no‐observed effect level, NOEL) of ZEA impaired mouse spermatogenesis and decreased mouse semen quality. The purpose of the current investigation was to explore the impacts of low‐dose ZEA on spermatogenesis in the offspring after prenatal exposure and the underlying mechanisms. And it demonstrated that prenatal low‐dose ZEA exposure disrupted the meiosis process to inhibit the spermatogenesis in offspring and even to diminish the semen quality by the decrease in spermatozoa motility and concentration. The DNA methylation marker 5hmC was decreased, the histone methylation markers H3K9 and H3K27 were elevated, and oestrogen receptor alpha was reduced in the offspring testis after prenatal low‐dose ZEA exposure. The data suggest that the disruption in spermatogenesis by prenatal low‐dose ZEA exposure may be through the modifications on epigenetic pathways (DNA methylation and histone methylation) and the interactions with oestrogen receptor signalling pathway. Moreover, in the current study, the male offspring were indirectly exposed to low‐dose ZEA through placenta and the spermatogenesis in offspring was disrupted which suggested that the toxicity of ZEA on reproductive systems was very severe. Therefore, we strongly recommend that greater attention should be paid to this mycotoxin to minimize its adverse impact on human spermatogenesis.