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Glycine alleviates ovarian granulosa cell ferroptosis induced by ERα-mediated internalization of polystyrene microplastics
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Researchers found that polystyrene microplastic exposure in mice triggers ferroptosis (iron-mediated cell death) in ovarian granulosa cells via ERα-mediated internalization and YAP1-ACSL4 signaling, and demonstrated that the amino acid glycine can restore iron homeostasis and alleviate this reproductive toxicity.
Polystyrene microplastics (PSs), pervasive environmental contaminants found in food and human tissues, pose an emerging threat to reproductive health. Elucidating the mechanisms underlying PS-induced toxicity and identifying effective interventions to mitigate adverse effects are therefore critically important. Here, our findings demonstrated that PS exposure in 5-week-old female SPF Kunming mice leads to decreased serum hormone levels and reduced transzonal projections. Furthermore, this study revealed that PS-induced ferroptosis in ovarian granulosa cells. Mechanistically, ERα-mediated PS internalization led to activation of the YAP1-ACSL4 signalling and subsequent lipid peroxidation. Moreover, we demonstrated that glycine effectively alleviate PS-induced ferroptosis by modulating lysosome-dependent ferritin degradation in a PAT1-dependent manner, thereby restoring iron homeostasis. Taken together, these findings revealed that PS exposure triggers ACSL4 overexpression and iron overload in ovarian granulosa cells, whereas glycine restored iron homeostasis via lysosome-mediated ferritinophagy. This study provides critical insights into the reproductive health risks of PS exposure and offers a potential intervention strategy.
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Researchers showed that polystyrene nanoplastics induce ferroptosis — an iron-dependent form of cell death — in mouse sperm precursor cells by promoting the ubiquitin-tagged degradation of the iron-export protein ferroportin1, causing iron to accumulate inside cells, driving lipid peroxidation and mitochondrial damage.
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Researchers found that polystyrene nanoplastics trigger ferroptosis — a form of iron-dependent cell death driven by fat oxidation — in pig egg cells, disrupting their maturation and reproductive viability. This finding raises concerns about nanoplastic exposure potentially impairing fertility by damaging the eggs needed for reproduction.
Ferroptosis: First evidence in premature duck ovary induced by polyvinyl chloride microplastics
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Researchers discovered that polyvinyl chloride microplastics caused premature ovarian damage in ducks through a cell death process called ferroptosis, which involves iron-dependent oxidative damage. Higher microplastic concentrations led to iron accumulation, increased oxidative stress, and structural damage to ovarian tissue. This is the first evidence linking microplastic exposure to ferroptosis in the avian reproductive system.
Polystyrene microplastics cause granulosa cells apoptosis and fibrosis in ovary through oxidative stress in rats
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Researchers exposed female rats to polystyrene microplastics at different concentrations for 90 days and examined the effects on their ovaries. The study found that microplastic exposure caused cell death and tissue scarring in the ovaries through oxidative stress, suggesting that microplastics may have implications for female reproductive health.
Internalized polystyrene nanoplastics trigger testicular damage and promote ferroptosis via CISD1 downregulation in mouse spermatocyte
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Researchers found that polystyrene nanoplastics cause testicular damage in mice through a cell death process called ferroptosis. The nanoplastics triggered the breakdown of iron-storage proteins and reduced levels of a protective mitochondrial protein called CISD1 in sperm cells. The study suggests that nanoplastic exposure may contribute to male reproductive harm by driving excess iron into mitochondria.
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When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.