Nickel chloride induces spermatogenesis disorder by testicular damage and hypothalamic-pituitary-testis axis disruption in mice

Abstract

As a common environmental pollutant, nickel chloride (NiCl₂) poses serious threat to human and animals health. NiCl₂ has adverse effects on reproductive function in male, however, the underlying mechanisms are not fully illuminated. In this study, 64 male ICR mice were divided into four groups (8 mice per each period/ group), in which mice orally administrated with 0, 7.5, 15 or 30 mg/kg body weight for 14 or 28 consecutive days, respectively. The results showed that the sperm concentration (12.95%, 29.78% and 37.63% -) and sperm motility (19.79%, 34.88% and 43.10%) were dose-dependent significantly reduced, and the total sperm malformation rates (110.15%, 206.84% and 292.27%) were dose-dependent significantly elevated in the 7.5, 15 and 30 mg/kg NiCl₂ treatment groups (vs control at 28 days), respectively (P < 0.05). Meanwhile, NiCl₂ also decreased the relative weights of testis and epididymis and caused histopathological lesions of testis and epididymis. Furthermore, serum testosterone levels were significantly decreased after NiCl₂ treatment. And the findings showed that NiCl₂ down-regulated the expression of LH-R, StAR, P450scc, 3β-HSD, 17β-HSD, ABP and INHβB in the testis, however, the relative genes in the hypothalamus (Kiss-1, GPR54 and GnRH) and pituitary (GnRH-R, LHβ and FSHβ) did not exhibit noticeable change. In summary, NiCl₂ induced spermatogenesis disorder by testicular damage and hypothalamic-pituitary-testis axis disruption in mice, and only impaired the genes on the testis of HPT axis.

Keywords: Hypothalamic-pituitary-testis axis; NiCl(2); Spermatogenesis; Testis; Testosterone.