2021•JBRAOpen access

Protective effects of selenium on Bisphenol A-induced oxidative stress in mouse testicular mitochondria and sperm motility

Zeinab Rafiee, Fatemeh Rezaei‐Tazangi, Leila Zeidooni, Hadis Alidadi, Layasadat Khorsandi

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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.

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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.

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Available 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.

Key concepts: Oxidative stress, Sperm motility, Malondialdehyde, Sperm, Reactive oxygen species, Superoxide dismutase, Andrology, Mitochondrion

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Protective effects of selenium on Bisphenol A-induced oxidative stress in mouse testicular mitochondria and sperm motility — Research Paper | ScholarLens