Triclosan Exposure Induced Oxidative Stress and Testosterone Synthesis

Objective To investigate effects of triclosan (TCS) on the testicular morphology, steroid hormone levels, and hormone receptor expressions in pubertal male rats, and explore potential mechanisms of TCS-mediated inhibitions of testosterone biosynthesis in rats.

Methods Twenty-four Sprague-Dawley rats were selected and gavaged continuously with TCS for 31 days. Histopathologic alterations in rat testes were assessed by hematoxylin and eosin (HE) staining analyses. Gonadotropin releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T) levels in rat plasma were determined using enzyme-linked immunoabsorbent assay kits. Glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) levels in rat testicular tissue were assayed using biochemical kits.

Results TCS led to abnormal changes of testicular histomorphology of exposed rats. Moreover, plasma levels of T and LH decreased in TCS-treated groups. After TCS exposure, activities of SOD and CAT decreased while the level of MDA increased in rat testes. In addition, TCS exposure inhibited mRNA levels of androgen receptor (AR) and luteinizing hormone receptor (LHR), and meanwhile declined protein expressions of 5α-reductases (SRD5A1 and SRD5A2) in rat testes.

Conclusion These findings suggest that TCS disturbs the homeostasis of the hypothalamic-pituitary-testis axis to reduce plasma testosterone levels, and the decrease of 5α-reductase protein expressions may be an underlying compensatory mechanism in the body.