We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Testicular mitochondrial redox imbalance and impaired oxidative phosphorylation underlie microplastic-induced testicular dysfunction in Wistar rats
Summary
Researchers investigated how polyethylene microplastics affect male reproductive function in rats by examining testicular mitochondrial health. The study found that microplastic exposure disrupted mitochondrial redox balance and impaired oxidative phosphorylation in testicular tissue, providing mechanistic evidence for how microplastics may contribute to male reproductive toxicity.
Polyethylene microplastics (PE-MPs), now pervasive environmental contaminants, have been implicated in reproductive toxicity, but their mechanistic effects on testicular function remain poorly defined. This study investigates the mechanistic basis of PE-MPs-induced male reproductive toxicity in a rodent model (Wistar rats), with a specific focus on testicular mitochondrial redox homeostasis and oxidative phosphorylation. By integrating mitochondrial bioenergetics, redox signaling, histopathology, and reproductive endpoints, the work advances mechanistic toxicology insights relevant to environmental reproductive health. Fifteen male rats were randomly divided into three groups: control, and PE-MPs treated groups receiving 15 or 60 mg/kg body weight orally for 28 days. Testicular mitochondria were isolated to evaluate activities of tricarboxylic acid (TCA) cycle enzymes, citrate synthase (CS), isocitrate dehydrogenase (IDH), succinate dehydrogenase (SDH), and malate dehydrogenase (MDH), as well as respiratory chain complexes I-IV. Mitochondrial redox balance indices, including malondialdehyde (MDA), myeloperoxidase (MPO), reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD), were also assessed. PE-MP exposure induced a dose-dependent suppression of TCA cycle and electron transport activities, with CS and SDH inhibited by up to 50% at the highest dose suggesting a broad inhibition of electron transport and ATP synthesis. These mitochondrial impairments coincided with elevated MDA and MPO levels, and significant depletion of GSH, CAT, and SOD, indicating profound mitochondrial oxidative distress. These mitochondrial disturbances correlated with histological evidence of testicular degeneration and decreased testosterone levels. Collectively, the findings of this study highlight that PE-MPs compromise testicular bioenergetics and function by disrupting testicular oxidative phosphorylation and redox homeostasis, leading to mitochondrial dysfunction, structural degeneration, and impaired steroidogenesis, providing mechanistic insight into microplastic-induced male infertility. Understanding this bioenergetic collapse provides a biochemical framework for assessing the reproductive toxicity of microplastics and underscores the urgency of mitigating their exposure in vulnerable populations.
Sign in to start a discussion.
More Papers Like This
Determination of Biological and Molecular Attributes Related to Polystyrene Microplastic-Induced Reproductive Toxicity and Its Reversibility in Male Mice
Researchers exposed male mice to polystyrene microplastics through drinking water and found that the particles caused mitochondrial damage in testicular tissue, including reduced membrane potential and disrupted energy production. This mitochondrial dysfunction led to decreased sperm quality, likely driven by oxidative stress. Importantly, the study found that sperm quality recovered after one to two spermatogenic cycles without further exposure, suggesting that reproductive toxicity from microplastics may be reversible.
Microplastics and male reproductive system: A comprehensive review based on cellular and molecular effects
This comprehensive review examines how microplastics affect the male reproductive system at cellular and molecular levels, drawing on studies from multiple scientific databases. Researchers found that microplastics can damage testicular structure and function, impair spermatogenesis, and disrupt sperm parameters through mechanisms including oxidative stress, inflammation, and activation of cell death pathways. The review highlights that microplastics reduce ATP production and trigger signaling cascades that may contribute to male fertility problems.
A meta-analysis-based adverse outcome pathway for the male reproductive toxicity induced by microplastics and nanoplastics in mammals
This meta-analysis of 39 studies mapped the adverse outcome pathway for microplastic and nanoplastic-induced male reproductive toxicity in mammals. Increased reactive oxygen species triggers a cascade of cellular damage including mitochondrial dysfunction, sperm DNA damage, and disrupted hormone signaling, ultimately leading to reduced sperm quality, impaired spermatogenesis, and decreased testosterone levels.
Polystyrene Microplastics Disrupt Spermatogenesis through Oxidative Stress in Rat Testicular Tissue
Male Wistar rats orally administered polystyrene microplastics showed excessive oxidative stress in testicular tissue across all exposure groups, with spermatogenesis impairment and reduced fertility correlating with dose, demonstrating reproductive toxicity in a mammalian model.
Polystyrene microplastics induce male reproductive toxicity in mice by activating spermatogonium mitochondrial oxidative stress and apoptosis
A mouse study found that polystyrene microplastics significantly reduced sperm count and motility while increasing sperm deformities. The damage was caused by oxidative stress in the energy-producing mitochondria of sperm-forming cells, which triggered cell death -- raising concerns about microplastics' potential impact on male fertility.