Testosterone propionate ameliorates oxidatve stress and inflammation in nicotine-induced testicular toxicity

Abstract

BACKGROUND: Nicotine (NICO) is a major constituent of cigarette smoke and has been associated with adverse effects on the testes and male reproductive profile. 
AIMS AND OBJECTIVES: This study was initiated to investigate the effects of testosterone (TES) propionate in NICO‑induced testicular toxicity in rats by investigating the quantitative localization and intensity of immune expression of cyclooxygenase‑2 (COX‑2) and Ki‑67. 
MATERIALS AND METHODS: Eighteen adult Wistar rats were randomly divided into three groups as follows: Group A: NICO only; Group B: NICO+TES propionate (NICO+TES); and Group C: Normal Control. 0.8 mg/kg body weight of NICO and 2.5 mg/kg of TES propionate were administered, respectively, for 30 days after which the rats were sacrificed, and the testes were processed for antioxidant enzyme assay and immunohistochemical analysis. 
RESULTS: Immunohistochemical study showed elevated COX‑2 immunoexpression in the germinal epithelium of the NICO group relative to the NICO+TES and control groups. Ki‑67 was expressed in the spermatozoa of all experimental groups. The primary spermatocytes of NICO+TES and control groups additionally tested positive for Ki 67. The results also showed a higher level of oxidative stress markers in the NICO group compared to the NICO+TES and control groups. 
CONCLUSION: These findings indicate that NICO toxicity in the testes is mediated through inflammation and apoptosis as well as induction of oxidative stress; and that TES propionate ameliorates the severity of toxicity induced by NICO in rat testes by reducing the inflammation and oxidative stress.