Genetic, biochemical and histopathological evaluations of thymoquinone on male reproduction system damaged by paclitaxel in Wistar rats.

This study was aimed to evaluate therapeutic effects of thymoquinone on male reproductive damages induced by paclitaxel. Forty-eight male rats were divided; control, paclitaxel (4 mg/kg), paclitaxel + thymoquinone (1.25, 2.5 and 5 mg/kg) and thymoquinone (1.25, 2.5 and 5 mg/kg). Paclitaxel and thymoquinone were administrated intraperitoneally for 4 and 14 days respectively. Then, the testes were removed for H&E staining, sperm parameters and apoptotic genes expression assessments. Serum levels of nitric oxide, total antioxidant capacity and testosterone were evaluated, and sperm DNA fragmentation was assessed. Paclitaxel significantly (p < .05) increased nitric oxide, decreased total antioxidant capacity and reduced testosterone levels than control group. Sperm motility, viability and count were significantly (p < .05) reduced in paclitaxel group than control. Co-administration of thymoquinone + paclitaxel caused decreased levels of nitric oxide and increased total antioxidant capacity, testosterone levels and reproductive parameters than paclitaxel group significantly (p < .05). Paclitaxel significantly (p < .05) increased caspase-3 and p-53 and decreased Bcl-2 genes expression than control. Sperm DNA fragmentation index was also increased significantly (p < .05) in paclitaxel group than control, and this value was decreased in whole doses of paclitaxel + thymoquinone groups than paclitaxel. Thymoquinone can alleviate the side effects of paclitaxel on the male reproductive system.