Ginger reserves testicular spermatogenesis and steroidogenesis in difenoconazole-intoxicated rats by conducting oxidative stress, apoptosis and proliferation.

Abstract

Difenoconazole, a triazole fungicide, can induce reproductive toxicity in aquatic species, but the probable mechanisms of this hazard in mammals are not formally reported. Here, we have examined the possible ameliorative efficiency of the ginger aqueous extract against the reproductive toxicity of difenoconazole in male rats. Thirty-six animals were equally divided into six groups: control, ginger aqueous extract (50mg/kg), difenoconazole (15mg/kg), difenoconazole (30mg/kg) and ginger co-treated with two doses of difenoconazole. Difenoconazole markedly decreased sperm count, motility and normality percentage, together with the Johnson score. Difenoconazole also significantly reduced serum testosterone, luteinizing hormone and follicle-stimulating hormone levels, as well as the activities of testicular steroidogenic acute regulatory protein and 17 β-hydroxysteroid dehydrogenases. Furthermore, difenoconazole brought a significant decrease in the testicular activity of catalase, but it increased the activity of glutathione peroxidase. Moreover, difenoconazole upregulated the testicular transcripts of Bax and caspase-3, increased Ki-67 immunoreactivity and induced histoarchitecture alterations plus DNA damage. Remarkably, ginger co-treatment preserved sperm toxicity, restored hormone profiles, increased steroidogenic activity and prevented oxidative injury-promoted testicular apoptosis. In conclusion, phenolic acids and flavonoids of ginger can reserve spermatogenesis and steroidogenesis in difenoconazole-intoxicated rats by improving testicular redox status, inhibiting apoptosis and refining proliferation capacity.