The Effects of Microplastics and Trace Elements on Ovarian Function and Pathology: A Literature Review
5 affiliations
- 1Department of Forensic Medicine, Medical University of Lublin, Jaczewskiego 8b, 20-090 Lublin, Poland
- 2Doctoral School, Medical University of Lublin, Chodźki 7, 20-093 Lublin, Poland
- 3Department of Correct, Clinical and Imaging Anatomy, Medical University of Lublin, ul. Jaczewskiego 4, 20-090 Lublin, Poland
- 4Student Scientific Society of Correct, Clinical and Imaging Anatomy, Medical University of Lublin, ul. Jaczewskiego 4, 20-090 Lublin, Poland
- 5Department of Analytical Chemistry, Medical University of Lublin, Chodźki 41 (Collegium Pharmaceutcum), 20-093 Lublin, Poland
Abstract
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., Steroidogenic acute regulatory protein (StAR), CYP11A1, CYP19A1) 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.
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BibTeX
@article{brylinski2026effects,
title = {{The Effects of Microplastics and Trace Elements on Ovarian Function and Pathology: A Literature Review}},
author = {Łukasz Bryliński and Katarzyna Brylińska and Jolanta Sado and Kacper Kraśnik and Miłosz Smyk and Olga Komar and Filip Woliński and Michał Flieger and Jolanta Flieger and Grzegorz Teresiński and Alicja Forma and Jacek Baj},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = sep,
doi = {10.3390/ijms27188306},
url = {https://www.mdpi.com/1422-0067/27/18/8306},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Effects of Microplastics and Trace Elements on Ovarian Function and Pathology: A Literature Review
AU - Łukasz Bryliński
AU - Katarzyna Brylińska
AU - Jolanta Sado
AU - Kacper Kraśnik
AU - Miłosz Smyk
AU - Olga Komar
AU - Filip Woliński
AU - Michał Flieger
AU - Jolanta Flieger
AU - Grzegorz Teresiński
AU - Alicja Forma
AU - Jacek Baj
PY - 2026
DA - 2026/09/18
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27188306
UR - https://www.mdpi.com/1422-0067/27/18/8306
AB - 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., Steroidogenic acute regulatory protein (StAR), CYP11A1, CYP19A1) 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.
SN - 1422-0067
ER -