Prenatal microplastic exposure-induced testicular developmental toxicity and its long-term hazards in male rat offspring.

Authors

Linguo Pei, Yuanyuan Zhang, Wenjuan Zhang, Wei Wang, Wenyu Jin

Published in

Toxicology and industrial health. Pages 7482337261500552. Oct 18, 2026. Epub Oct 18, 2026.

Abstract

The pervasive environmental presence of microplastics (MPs) raises concerns regarding their potential impacts on reproductive health, particularly in the context of prenatal exposure. This study aimed to establish a polystyrene microplastics (PS-MPs) exposure model in pregnant rats and to investigate the subsequent effects on the growth, hormonal profiles, steroidogenic enzyme expression, and testicular histology of male offspring from birth to adulthood. Pregnant rats were administered PS-MPs at doses of 1 mg/kg/day (MPs-L) and 10 mg/kg/day (MPs-H) during gestational days 10-20. Results indicated that birth weights in the MPs-L and MPs-H groups decreased to 88.7% and 85.3% of controls, respectively, with persistent intrauterine growth restriction and no catch-up growth observed. Testicular morphology analysis revealed significant reductions in testicular area and diameter in neonatal rats, alongside adult testicular index decline and altered sperm parameters. Hormonal assessments showed concentration-dependent decreases in serum testosterone levels during neonatal and adult stages, coupled with reduced luteinizing hormone levels in adults, indicating a non-classical "low testosterone-low luteinizing hormone" phenotype. Molecular evaluations demonstrated selective suppression of key steroidogenic genes (Star and 3β-Hsd) in neonatal and adult testicular tissues, while Leydig cell counts were significantly diminished. In conclusion, prenatal exposure to MPs had long-lasting repercussions on Leydig cell functionality and the spermatogenic environment, leading to dual structural and endocrine impairments that may have critical implications for male reproductive health. Future studies should further explore the mechanisms underpinning these effects and potential interventions.

PMID:
42893446
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.

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