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Synergistic nanotoxicology: Mitochondrial ROS-driven mitochondrial damage and oxidative stress underlie polylactic acid nanoplastics and silica nanoparticle-induced testicular dysfunction
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Tiny plastic particles (from biodegradable plastics like PLA) and silica nanoparticles (a common food additive) are both things people encounter regularly, and this study found that when mice were exposed to both together, the damage to testicular tissue and sperm production was worse than either one alone. The combo overwhelmed the cells' mitochondria (their energy factories), causing a buildup of harmful molecules that damaged reproductive tissue, though a targeted antioxidant treatment reversed the effects in mice. While this is animal research and not a direct proof of harm in humans, it's an early warning sign that combined exposure to different
Polylactic acid (PLA) and synthetic amorphous silica (SAS), both extensively utilized in food-related applications, raise significant toxicological concern owing to their co-exposure potential to humans. Previous studies have shown that PLA and SAS can lead to reproductive toxicity. However, the combined reproductive effects and underlying mechanisms in mammalian are still indistinct. In this study, we investigate the combined toxicity of PLA nanoplastics (PLA NPs) and silica nanoparticles (SiNPs) on male reproduction. The co-exposure to PLA NPs and SiNPs significantly enhanced reproductive toxicity, including testicular structural damage, spermatogenic disturbance and sex hormone disorder. Furthermore, PLA NPs and SiNPs synergistically caused severe mitochondrial damage and generated excessive reactive oxygen species (ROS), subsequently inhibiting the Kelch-like ECH-associated protein 1/ Nuclear factor erythroid 2-related factor 2 pathway to exacerbate oxidative stress. Mitochondrial-targeted antioxidant intervention effectively normalized oxidative stress and reproductive damage. These results demonstrated that PLA NPs and SiNPs synergistically aggravated testicular toxicity in mice by inducing mitochondrial ROS production resulting in mitochondrial damage as well as enhancing oxidative stress. Our study provides a foundation for future studies on the mechanism of toxicity in mammals by synergistic exposure to PLA NPs and SiNPs.
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Biochemical, Histological and Molecular Docking into the Impact of Polystyrene Nanoplastics on Antioxidant Enzymes and Testicular Health in Rats
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Tiny plastic particles called nanoplastics, found widely in our environment, may harm male fertility, according to a new rat study. Rats exposed to higher doses of these plastics showed weakened antioxidant defenses and physical damage to testicular tissue, including fewer developing sperm cells. While this research was done in rats, not humans, it adds to growing concerns that the microplastics and nanoplastics we're routinely exposed to through food, water, and air could pose risks to reproductive health.
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Prenatal exposure to polystyrene nanoplastics caused testicular development toxicities and relative mechanisms in male offspring mice from embryo to adulthood
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Scientists exposed pregnant mice to nanoplastics (tiny plastic particles found in our environment, blood, and even placentas) and found their male offspring had slowed growth before birth, hit puberty earlier, and had reduced fertility as adults. The nanoplastics appeared to disrupt key genes and cells needed for normal testicle development and hormone production. While this is animal research, it adds to growing evidence that plastic exposure during pregnancy could affect a baby's reproductive development later in life.
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