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Protective effect of lycopene on testicular toxicity induced by Benzo[a]pyrene intake in rats
- Xu, Anran, Wang, Jianye, Wang, Haiyu, Sun, Yanqing, Hao, Tianyu
- Toxicology 2019
- Sertoli cells, adults, antioxidant activity, apoptosis, benzo(a)pyrene, blood serum, calcium, caspase-3, epididymis, gap junctions, genes, laboratory animals, lycopene, males, oxidants, oxidative stress, protective effect, rats, reproductive toxicology, sperm concentration, sperm motility, spermatozoa, staining, testosterone, toxicity
- Benzo[a]pyrene (BaP) stimulates male reproductive toxicity. In this study, we want to examine the ameliorative potential of Lycopene (LYC) on BaP-induced testicular toxicity. Adult male Wistar rats were segregated into 5 groups: Control, LYC, BaP, BaP + LYC and BaP + PQ7. Sperm parameters, testosterone level, oxidant and antioxidant parameters were determined. MRNA and protein abundances of key genes were analyzed. Cell death and apoptosis were assessed by trypan blue exclusion and Annexin V-FITC staining assay, respectively. LYC inhibited BaP-caused decrease in sperm motility and epididymal sperm concentration, and increase in head, tail and total abnormal sperm rate. LYC inhibited BaP-caused decrease in testosterone level in serum and intratesticular fluids. LYC protected germ cells from BaP-caused oxidative stress. LYC also prevented BaP-caused germ cell death and apoptosis by inhibiting apoptotic pathway. Besides, LYC ameliorated BaP-mediated gap-junction dysfunction of sertoli cells, as shown by the inhibited sertoli cell death and apoptosis, the upregulation of Bcl2 and Cx43, the downregulation of Cleaved Caspase 3, Bax and CaM, and the decrease in Ca2+ level. LYC ameliorated BaP-caused testicular damage via inhibiting oxidative stress and apoptosis, and relieving the gap-junction dysfunction of sertoli cells.