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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).
Summary
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.