Lipoic acid abates testis lead accumulation, sperm-endocrine deficits, testicular oxidative inflammation and apoptosis and modulates gene expression of Bax and Bcl-2 in rats

The current study explored whether ALA could prevent testis Pb accumulation and Pb-induced oxidative testicular toxicity in rats. Adult male rats were randomly divided and administered ALA (25 mg/kg/day) and/or Pb (Pb acetate, 20 mg/kg/day) in Control group, ALA group, Pb group, and ALA + Pb group for 4 weeks consecutively. Pb exposure significantly increased Pb accumulation in the testes and blood of Pb-exposed rats compared to the control. Pb caused marked deficits in sperm count, motility along with elevated abnormal sperm cells, while serum testosterone, follicle stimulating hormone (FSH) and leutenizing hormone (LH) levels reduced prominently in comparison to the control. It remarkably depressed the testicular activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), as well as levels of interleukin-4 (IL-4) and interleukin-10 (IL-10), whereas malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-& alpha;), and interleukin-6 (IL-6) increased significantly compared to the control. The levels of caspase-3, capsase-9, and the PCR gene expression of Bax and Bcl2 were adversely altered with alterations in testis histology. Interestingly, the co-treatment with ALA blocks Pb accumulation in the testis and blood. It inhibited the Pb-induced alterations in reproductive indices and reversed the oxidative stress-mediated inflammatory stress, apoptotic signaling and histopathological abrasions. The findings reveal that ALA could abrogate Pb-induced testicular toxicity through blocking testicular oxidative inflammation and apoptosis in rats.