1. Academic Validation
  2. Oral exposure to phenanthrene during gestation disorders endocrine and spermatogenesis in F1 adult male mice

Oral exposure to phenanthrene during gestation disorders endocrine and spermatogenesis in F1 adult male mice

  • Ecotoxicol Environ Saf. 2024 Jul 15:280:116566. doi: 10.1016/j.ecoenv.2024.116566.
Jiaojiao Guo 1 Zongxuan Yang 2 Jun Wang 2 Nan Liang 2 Yunshu Shi 2 Jiameng Zhong 2 Xu Zhang 2 Yu Hu 2 Buhe Nashun 3
Affiliations

Affiliations

  • 1 State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot, China; Inner Mongolia Engineering Technology Research Center of Germplasm Resources Conservation and Utilization, Hohhot, China. Electronic address: gjjlife@imu.edu.cn.
  • 2 State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot, China.
  • 3 State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot, China. Electronic address: bnashun@imu.edu.cn.
Abstract

Phenanthrene (Phe), a typical low-molecular-weight polycyclic aromatic hydrocarbon (PAH) of three benzene rings, is one of the most abundant PAHs detected in daily diets. Pregnant women and infants are at great risk of Phe exposure. In the present study, Phe was administered to pregnant mice at a dose of 0, 60, or 600 μg/kg body weight six times, and the F1 male mice showed significant reproductive disorders: the testicular weight and testis somatic index were significantly reduced; the levels of serum testosterone, GnRH and SHBG were increased, while the FSH levels were reduced; histological analysis showed that the amount of Sertoli cells and primary spermatocytes in seminiferous tubules was increased, while the amount of secondary spermatocytes and spermatids were decreased in Phe groups. The protein levels of PCNA and Androgen Receptor were reduced. Differently expressed genes in the testis screened by RNA sequence were enriched in antioxidant capacity, reproduction et al.. Further biochemical tests confirmed that the antioxidant capacity in the F1 testis was significantly inhibited by treatment with Phe during pregnancy. Those results suggested that gestational Phe exposure disordered hypothalamic-pituitary-gonadal (HPG) Hormones on the one hand, and on the Other hand reduced testicular antioxidant capacity and further arrested cell cycle in F1 adult male mice, which co-caused the inhibition of spermatogenesis.

Keywords

Gestational exposure; Phenanthrene; Polycyclic aromatic hydrocarbons (PAHs); Reproductive disorders; Spermatogenesis retardation.

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