Adverse effects of neonatal exposure to 3,3′,4,4′,5,5′‐hexachlorobiphenyl on hormone levels and testicular function in male Sprague–Dawley rats

Abstract

In this study, we investigated the time-course changes of hormone levels and sperm numbers in male Sprague-Dawley (SD) rats after neonatal exposure to 3,3',4,4',5,5'-hexachlorobiphenyl (PCB169). Neonatal rats were given (through oral gavages) doses of 0, 0.025, 0.25, or 0.5 mg/kg-day of PCB169 in corn oil from postnatal day 1 (PND1) to PND7. The rats were sacrificed at PND8, PND21, and PND90. PCB169 exposure was confirmed by the marked induction of liver CYP1A1 mRNA expression at these three time points. The testicular daily sperm production and the sperm counts of the epididymis cauda significantly decreased at PND90 compared to that of control. Although reductions in serum thyroxine and triiodothyronine levels occurred at all these three time points and at both PND21 and PND90, respectively, the mRNA expression of testicular thyroid hormone receptor α1 was suppressed significantly only at PND8. The serum and testicular testosterone (T) levels declined markedly at PND90 compared to the controls, but there was no effect at PND21. The mRNA expression of testicular steroidogenic factor 1 was inhibited markedly at the three time points, whereas those of StAR, P450c17, P450scc, and 3β-HSD were suppressed significantly only at PND90 relative to the controls. PCB169 treatment had no effects on pituitary follicle-stimulating hormone and luteinizing hormone levels and on their receptors' expression in the testes. These results indicate that neonatal exposure to PCB169 damages hormone levels and testicular function in the long-term, resulting in persistent hypothyroidism and decreases in adult T levels and sperm counts.

Relationships of Polychlorinated Biphenyls and Dichlorodiphenyldichloroethylene ( p,p’ -DDE) with Testosterone Levels in Adolescent Males

“…These results are consistent with experimental studies in animals that found endocrine-disrupting chemicals, such as PCBs and p,p´- DDE, modified serum testosterone levels (Ahmad et al 2003; Andric et al 2000; Kovacevic et al 1995; Xiao et al 2011), and with studies of humans that found associations consistent with endocrine modification due to those exposures (Croes et al 2009; Dhooge et al 2011; Goncharov et al 2009; Persky et al 2001; Richthoff et al 2003; Turyk et al 2006). …”

“…These studies have produced evidence of both stimulated and decreased testosterone in relation to marker PCBs and pollution, but no associations with p,p´- DDE (Croes et al 2009; Den Hond et al 2002; Dhooge et al 2011). Finally, a study of neonatal hexachlorobiphenyl exposure in rats found decreased adult serum testosterone levels (Xiao et al 2011). …”

In utero and childhood DDT, DDE, PBDE and PCBs exposure and sex hormones in adolescent boys: The CHAMACOS study

“…PCB exposure studies have demonstrated conflicting relationships with male hormones in both animal (Wakui et al 2010; Xiao et al 2011; Xu et al 2013; Zhu et al 2013) and human studies. For example, in a cohort of boys with higher prenatal exposure to PCBs during the Yucheng incident in 1978–79 (n=47) and unexposed controls (n=49), exposed boys who were at puberty (≥13 years old) had lower T levels and higher estradiol and FSH levels (non-significant) compared to controls, but there was no difference in boys < 13 years; there were also no differences in LH levels (Hsu et al 2005).…”

Effects of Polychlorinated Biphenyls 28, 30 and 118 on Bovine Spermatozoa In Vitro

“…; Xiao et al. ); act as tumour promoter by alternating/inhibiting gap junctional intercellular communication (Satoh et al. ) which was referred for its important role for male reprotoxicity (Cai et al.…”

“…() demonstrated that the neonatal exposure to PCBs has been reported to cause enlarged testis and increased testicular sperm counts associated with Sertoli cell changes; whereas hypothyroidism induced by exposure in early life stages result in decrease of testosterone level and testicular damage (Xiao et al. ).…”