Nutritional supplementation of D-Ribose-L-Cysteine suppresses oxidative stress, spermatogenesis and steroidogenesis recovery in rats exposed to mercury chloride: histomorphometry and biochemical evidence

oleh: Sunday A. Adelakun, Babatunde Ogunlade, Obinna P. Fidelis, Adewale A. Ajao

Format: Article
Diterbitkan: Elsevier 2021-09-01

Deskripsi

Background: Mercury chloride (HgCl2) is known to cause reproductive dysfunction. The negative effects may be ameliorated with the use of certain antioxidants. Present study focused on impact of D-Ribose-L-Cysteine (DRLC) on mercury chloride-induced testicular toxicity in male rats. Materials and methods: Forty-eight (48) adult male Sprague-Dawley rats weighing 150-200g randomized into six groups of eight (n=8) rats each. Group A treated with 1mg/Kg body weight (bwt) HgCl2; Group B received 30mg/Kg bwt of DRLC; Group C received 1mg/Kg bwt of HgCl2 and 30 mg/Kg bwt of DRLC; Group D received 1mg/Kg bwt of HgCl2 and 30mg/Kg bwt of Vit. C; Group E received 1mg/Kg bwt of HgCl2 and 30mg/Kg bwt of DRLC and 30 mg/Kg bwt of Vit. C; Group F served as control given normal saline orally for 8 weeks. Testicular histology, histomorphometry parameters, and other parameters such as sperm, luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone (TT), reduced glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) were investigated. Results: Administration of HgCl2 disorganized seminiferous epithelium and widened the hypocellular interstitium; significantly decrease the sperm quality, TT, FSH, LH, CAT, GPx, GSH, SOD, and increases the MDA compared to control group. Co-administration of HgCl2, DRLC and Vit.C decrease the MDA and increase hormonal and antioxidant level; improved sperm quality and restored testicular histopathological alterations. Conclusion: Intervening action of DRLC therefore, resulted in normal germinal cell layers, suppresses oxidative stress, spermatogenesis and steroidogenesis recovery in HgCl2 induced testicular toxicity.