ABSTRACT
OBJECTIVE: This study aimed to explore the impact of selenium (SE) on Bisphenol-A (BPA)-exposed sperm and isolated testicular mitochondria of mice. METHODS: Mouse sperm and isolated mitochondria were exposed to BPA (0.8 mM) and different concentrations of SE (50, 100, and 200 µM) for four hours. The viability of sperm and isolated mitochondria as well as the mitochondrial membrane potential (MMP) were evaluated. SOD (superoxide dismutase), GSH (glutathione), MDA (malondialdehyde), and ROS (reactive oxygen species) levels in testicular mitochondria were also examined. RESULTS: BPA concentration-dependently enhanced ROS and MDA levels in isolated mitochondria, while MMP and acclivity of GSH and SOD significantly reduced. BPA also considerably impaired spermatozoa survival and motility. SE concentration-dependently reduced mitochondrial oxidative stress, MMP, sperm survival, and total sperm motility. CONCLUSIONS: Our findings collectively suggested that SE concentration-dependently reversed BPA-caused mitochondrial toxicity and reduced sperm motility by suppressing oxidative stress.
Subject(s)
Selenium , Sperm Motility , Animals , Benzhydryl Compounds , Male , Mice , Mitochondria/metabolism , Oxidative Stress , Phenols , Selenium/metabolism , Spermatozoa/metabolismABSTRACT
OBJECTIVES: This study was performed to investigate the protective effects of taurine (2-aminoethanesulfonic acid, TAU) on oxidative stress in the isolated mouse testicular mitochondria, mitochondrial membrane potential (MMP), viability and motility of the exposed sperms to the BPA. METHODS: We treated epididymal spermatozoa obtained from mice and isolated mouse testicular mitochondria with BPA (0.8 mmol/mL) and various doses of TAU (5, 10, 30 and 50 µmol/L). We used the MTT assay and Rhodamine 123 uptake to assess sperm viability and MMP. We assessed the oxidative stress through measuring ROS (reactive oxygen species), MDA (malondialdehyde), GSH (glutathione), and SOD (super-oxide dismutase) levels in the testicular mitochondrial tissue. RESULTS: BPA significantly elevated ROS, MDA and MMP levels, and markedly reduced SOD and GSH levels in the isolated mitochondria. BPA also considerably impaired spermatozoa viability and motility. Pretreatment with 30 and 50 µmol/L of TAU could considerably suppressed mitochondrial oxidative stress, enhanced MMP, and improved sperm motility and viability. CONCLUSION: TAU may attenuate the BPA-induced mitochondrial toxicity and impaired sperm motility via decreasing oxidative stress.
