Volume 20, Issue 2 (May 2026)                   IJT 2026, 20(2): 124-129 | Back to browse issues page

Ethics code: This research has received ethical legislation number: No. 254/EC/KEPK/08/2023


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Janasti L, Sari R T, Aditya M R, Sulistomo H W. Reproductive Toxicity of Inhaled Polyethylene Microplastics: Oxidative Stress and Caspase-3–Mediated Apoptosis in the Ovaries of Female Wistar Rats. IJT 2026; 20 (2) :124-129
URL: http://ijt.arakmu.ac.ir/article-1-1563-en.html
1- Department of Midwifery, Universitas Bhakti Hasta Mulia Madiun, Madiun, Indonesia.
2- Department of Midwifery, Poltekkes Kemenkes Kalimantan Timur, Samarinda, Indonesia.
3- Department of Biomedical Sciences, Faculty of Medicine, Brawijaya University, Malang, Indonesia
4- Department of Pharmacology, Faculty of Medicine, Brawijaya University, Malang, Indonesia , hikmawan_ws@ub.ac.id
Abstract:   (161 Views)
Background: The increasing global production of plastics has led to widespread environmental contamination, including airborne microplastics capable of entering the respiratory tract, reaching systemic circulation, and inducing oxidative stress. This study aimed to assess the reproductive toxicity of sub-acute inhalation exposure to polyethylene (PE) microplastics on ovarian folliculogenesis, apoptosis, and oxidative stress in female Wistar rats (Rattus norvegicus).
Methods: Twelve adult female Wistar rats were randomly divided into control and experimental groups (n=6 each). The experimental group was exposed to aerosolized PE microplastics in a chamber for 4 h/day over 28 days. Ovarian tissues were examined for follicle counts (primary, secondary, antral, and atretic), caspase-3 expression in antral follicle granulosa cells, and oxidative stress markers by measuring the malondialdehyde to superoxide dismutase (MDA/SOD) ratio.
Results: The PE microplastic exposure significantly reduced the numbers of primary (p=0.0137), secondary (p=0.0053), and antral follicles (p=0.0033), while increasing atretic follicles (p=0.0062). Caspase-3 expression in antral follicle granulosa cells was markedly upregulated (p=0.0173). Additionally, the MDA/SOD ratio was significantly elevated (p=0.0043), indicating oxidative stress induction. These findings suggest that PE microplastic inhalation disrupts folliculogenesis through oxidative stress and apoptosis pathways.
Conclusion: Sub-acute inhalation of polyethylene microplastics induces oxidative stress and caspase-3–mediated apoptosis in ovarian tissue, leading to follicular depletion and potential reproductive toxicity.

 
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Type of Study: Research | Subject: General

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