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  3. Prenatal exposure to environmentally relevant levels of PAHs inhibits spermatogenesis in adult mice and the mechanism involved

Prenatal exposure to environmentally relevant levels of PAHs inhibits spermatogenesis in adult mice and the mechanism involved

  • Environ Pollut. 2024 Sep 6:362:124914. doi: 10.1016/j.envpol.2024.124914.
Kunlin Ou 1,  Siqi Zhang 2,  Xinxing Lei 3,  Xiao Liu 3,  Ningfang Zhang 3,  Chonggang Wang 4,  Xiaopeng Yuan 5
Affiliations

Affiliations

  • 1 Department of Laboratory Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, 518020, Guangdong, China; The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, 510630, China; State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
  • 2 State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China; National Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, Guangdong, 518112, China.
  • 3 Department of Laboratory Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, 518020, Guangdong, China.
  • 4 State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361005, China.
  • 5 Department of Laboratory Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, 518020, Guangdong, China. Electronic address: Yuanxp2001@126.com.
PMID: 39245200 DOI: 10.1016/j.envpol.2024.124914
Abstract

Polycyclic aromatic hydrocarbons (PAHs) are a class of contaminants that cannot be banned. Exposure to PAHs has been reported to alter spermatogenesis in mammals, but little is known about prenatal exposure to a mixture of PAHs on the reproductive toxicity of adult offspring. In this study, we investigated the associations between prenatal exposure to environmentally relevant levels of PAHs in mice and testicular dysfunction, including impaired spermatogenesis and steroid hormone dysfunction in male offspring on postnatal day 180. The percentage of testicular apoptotic cells was significantly increased, which was further verified by the up-regulated Bax protein. The expression of Ar and the Leydig cell marker Cyp11a1 was down-regulated, suggesting an impairment in the synthesis of steroid Hormones. DNA hypermethylation of the Tnp1 and Sohlh2 promoters suppresses transcriptional expression, consequently altering the sperm production process. This study shows that prenatal exposure to PAHs may induce long-term reproductive toxicity.

Keywords

Apoptosis; DNA methylome; Environmental endocrine disruptors; Polycyclic aromatic hydrocarbons; Spermatogenesis.

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