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The Effects of Microplastics and Trace Elements on Ovarian Function and Pathology: A Literature Review.
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This review pulls together existing research showing that microplastics and heavy metals like lead and mercury can damage the ovaries, disrupting hormones and speeding up egg reserve loss. Worse, when these pollutants combine, they may cause more harm together than either does alone, raising concerns about everyday environmental exposures and fertility.
The female reproductive system, particularly the ovary, exhibits a high sensitivity to the effects of environmental xenobiotics. This group of substances includes micro- and nanoplastics (MNPs) as well as trace elements. This literature review summarises the current knowledge on the individual and combined effects of MNPs and trace elements-including essential bioelements (zinc (Zn), selenium (Se), copper (Cu), chromium (Cr), manganese (Mn)) and toxic elements (cadmium (Cd), Lead (Pb), arsenic (As), mercury (Hg))-on ovarian physiology and clinical conditions such as polycystic ovary syndrome (PCOS), gonadal dysfunction and infertility. Essential trace elements play irreplaceable roles as enzyme cofactors (e.g., superoxide dismutase (SOD), glutathione peroxidase (GPX)) and transcriptional regulators; however, their biological action is confined to a narrow homeostatic window, within which both deficiency and excess disrupt cellular redox status and the hypothalamic-pituitary -gonadal axis. The effect of toxic heavy metals is different; these exhibit threshold-independent cytotoxic, genotoxic and endocrine-disrupting effects, inducing apoptosis of granulosa cells, endoplasmic reticulum stress and the silencing of steroidogenic genes (e.g., , , ) via epigenetic modifications, which accelerates the depletion of the ovarian reserve (measured by a decline in anti-Müllerian hormone (AMH)). Concurrently, MNPs overcome biological barriers and accumulate within the ovarian microenvironment, thereby inducing reactive oxygen species (ROS)-dependent apoptosis, NLR family pyrin domain-containing 3 (NLRP3) inflammasome-mediated pyroptosis, cytoskeletal disruption, and tissue fibrosis. A key element of this review is the identification of mechanistic convergence and potential toxic synergism between MNPs and heavy metals. Co-exposure enhances toxin retention within cells by inhibiting ATP-binding cassette (ABC) transporters, potentiates mitochondrial depolarisation, and activates protein kinase RNA-like endoplasmic reticulum kinase-eukaryotic translation initiation factor 2 alpha (PERK/eIF2α) stress signalling. Understanding these shared molecular pathways forms the basis for assessing multi-component risk in female reproductive toxicology and for developing targeted protective strategies.
More Papers Like This
Microplastics and Nanoplastics: Impacts on Female Reproductive Health, Ovarian Function, and Genitourinary Disorders
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Researchers review evidence that microplastics and nanoplastics accumulate in ovarian tissue, follicular fluid, and placental material, linking exposure to ovarian toxicity, hormonal disruption, reduced fertility, and elevated endometriosis risk through oxidative stress and inflammation-mediated pathways.
Microplastics and Nanoplastics: Impacts on Female Reproductive Health, Ovarian Function, and Genitourinary Disorders
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Researchers reviewed evidence showing microplastics and nanoplastics accumulate in ovarian tissue, follicular fluid, and the female genitourinary tract, where they trigger oxidative stress, endocrine disruption, and inflammation linked to reduced fertility, hormonal imbalance, and elevated risk of endometriosis.
Ovarian toxic effects of micro- and nanoplastics (Review)
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Tiny plastic particles called microplastics and nanoplastics have been found in the fluid surrounding eggs in women's ovaries, and this review pulls together existing research on how these particles may harm female fertility. Studies suggest these plastics can damage cells, disrupt hormones, and interfere with egg development, potentially reducing reproductive capacity—though most evidence so far comes from animal and lab studies rather than direct proof of harm in humans. Given how widespread plastic pollution has become, understanding these risks matters for anyone concerned about long-term fertility health.
Associations between concentrations of microplastics in follicular fluid and the risk of diminished ovarian reserve
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Researchers conducted a case-control study comparing microplastic levels in follicular fluid of patients with diminished ovarian reserve versus controls. Total microplastic abundance was significantly higher in the diminished ovarian reserve group (30.63 vs. 18.48 micrograms per gram), and elevated levels of polyethylene, polypropylene, and PVC were associated with reduced markers of ovarian function.
Impact of microplastics on female reproductive health: insights from animal and human experimental studies: a systematic review
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This systematic review of 15 experimental studies found that microplastic exposure significantly impairs ovarian function, decreases fertility rates, and disrupts hormone levels in female subjects. Several studies also reported negative effects on embryo development and offspring health, though study quality varied and more rigorous research is needed to confirm mechanisms.
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