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The SIRT gene family protects against oxidative stress and mitochondrial dynamic dysfunction induced by polystyrene nanoplastics in the ovaries of zebrafish (Danio rerio).
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Scientists found that tiny plastic particles (nanoplastics) can damage egg-producing tissue in zebrafish by disrupting a protective protein family called SIRTs, leading to cell stress and lower fertility. Boosting SIRT activity with a natural compound called resveratrol (found in foods like grapes and red wine) helped protect the fish's reproductive health, suggesting a possible way to counteract plastic-related damage. While this study was done in fish, it adds to growing evidence that the microplastics we're all exposed to daily could affect fertility, and hints at potential strategies to protect against it.
Micro- and nanoplastics (MNPs) are increasingly recognized as reproductive toxicants in aquatic organisms. Although numerous in vivo and in vitro studies have documented MNPs-induced reproductive damage, the underlying molecular mechanisms remain poorly understood. The SIRT protein family, a group of NAD-dependent histone deacetylases, plays important roles in regulation of reproductive function. This study aims to systematically elucidate the role of the SIRT proteins in mediating responses to polystyrene nanoplastics (PS-NPs) in female zebrafish. Adult female zebrafish were exposed to a range of PS-NPs concentrations. Exposure resulted in a dose-dependent reduction in the gonadosomatic index (GSI), fecundity, spawning capacity, fertilization rate and hatching rate of offspring. Significant changes in SIRT family gene expression were also observed. Molecular docking analysis indicated that PS-NPs can bind to and potentially inhibit all SIRT isoforms. To further investigate the role of SIRT proteins, zebrafish were co-exposed to 1.5 mg/L PS-NPs with the SIRT activator resveratrol (RSV) or the SIRT inhibitor nicotinamide (NAM). RSV significantly upregulated ovarian SIRTs expression, attenuated PS-NPs-induced increase in reactive oxygen species, and loss of mitochondrial membrane potential in ovarian follicles. In contrast, NAM suppressed SIRTs expression and exacerbated these mitochondrial and oxidative defects. qPCR revealed that RSV increased transcription of antioxidant genes (NRF, SOD, CAT, GPX) and mitochondrial fusion/biogenesis genes (OPA1, MFN1/2, TFAM), while decreasing the fission gene (DRP1), whereas NAM produced the opposite effects pattern. Together, these results implicate SIRT proteins in protecting ovarian function against PS-NPs toxicity and suggest SIRT modulation as a potential mechanism underlying MNP-induced female reproductive dysfunction.
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Polystyrene microplastics disrupt female reproductive health and fertility via sirt1 modulation in zebrafish (Danio rerio)
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This study found that polystyrene microplastics disrupted female reproductive health in zebrafish by interfering with a key protein called SIRT1 that regulates hormone production. Exposed fish showed changes in egg development, hormone levels, and ovarian tissue structure. Since the hormonal pathways affected are similar in humans, these findings raise concerns about how microplastic exposure might contribute to fertility problems in women.
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Researchers exposed female zebrafish to polystyrene nanoplastics before mating with unexposed males and found that maternal exposure at 100 μg/L reduced offspring hatching success and caused developmental defects in the F1 generation raised in clean water, demonstrating transgenerational toxicity via mitochondrial dysfunction.
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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.
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