摘要：Although known adverse effects of nicotine ex-posure on general health, it is largely consumed as cigarette smoking. Smoking has negative effects on the fertility in males; however, the molecular mech-anisms affected by nicotine are largely unclear. In this study, we aimed to investigate the effect of nic-otine on poly(ADP-ribose) polymerase(PARP)pathway in testicular damage. Twenty-four male C57BL/6J mice were arbitrarily categorized into three subgroups:control, sham(subcutaneous.0.9%sterile saline), and nicotine(subcutaneous,3 mg/kg/body weight/day)groups. After 14 days of twice-daily subcutaneous injections, the weights of the body and testes were measured. The levels of tes-tosterone, follicle-stimulating hormone(FSH), lute-inizing hormone(LH),cotinine(main metabolite of nicotine),and 8-OHdG(oxidative DNA damage in-dicator)in serum were determined using enzyme-linked immunosorbent assay(ELISA)method. Light microscopy was used for assessing sperm count and motility,as well as the histopathological analysis of testes and seminiferous tubule degeneration. Im-munohistochemical studies and real-time quantita-tive polymerase chain reaction(qPCR)were used for detecting the expressions of PARP-1 and caspase-3. The results showed that nicotine exposure signifi-cantly decreased the weight of mice and testes, re-duced the count and motility of sperm, while increas-ing the damage to seminiferous tubules. Nicotine ad-ministration significantly lowered the levels of se-rum FSH, LH, and testosterone; however, it in-creased the levels of8-OHdG and cotinine. Moreo-ver, the expressions of caspase-3 and PARP-1 signif-icantly increased. In conclusion, our results indicate that nicotinecauses damage to testicular tissue by ac-tivating the PARP-1 pathway.
