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Polystyrene microplastics induce blood-testis barrier disruption regulated by MAPK-Nrf2 signaling pathway in rats

Research Square (Research Square) 2021 5 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Shengda Li, Qimeng Wang, Hui Yu, Long Yang, Long Yang, Yiqing Sun, Ning Xu, Nana Wang, Zhimin Lei, Junyu Hou, Yinchuan Jin, Hongqin Zhang, Lianqin Li, Feibo Xu, Lianshuang Zhang

Summary

Researchers found that polystyrene microplastics (PS-MPs) disrupted the blood-testis barrier in male rats after 90 days of exposure, with higher doses (0.15 and 1.5 mg/d) causing significant spermatogenic cell apoptosis and reduced sperm motility through activation of the MAPK-Nrf2 signaling pathway.

Polymers
Body Systems
Models

Abstract As a persistent organic pollutant, microplastics (MPs) have been reported to induce sperm quantity decrease in male rats. However, the related mechanism remains obscure. Therefore, this study is intended to explore the effects of polystyrene microplastics (PS-MPs) on male reproduction and its related mechanism of blood-testis barrier (BTB) impairment. Thirty-two adult male Wistar rats were divided randomly into four groups fed with PS-MPs for 90 days at the dose of 0 mg/d (control group), 0.015 mg/d, 0.15 mg/d and 1.5 mg/d respectively. The present results have showed that PS-MPs exposure led to the damage of seminiferous tubule, resulted in apoptosis of spermatogenic cell and decreased the motility and concentration of sperm, while the abnormality of sperm was elevated. Meanwhile, PS-MPs could induce oxidative stress and activate p38 MAPK pathway and thus deplete the nuclear factor erythroid-2 related factor 2 (Nrf2). Noteworthily, the adverse effect of PS-MPs on BTB is only significant in 0.15 mg/d and 1.5 mg/d groups ,which demonstrated that high-dose PS-MPs exposure may lead to the destruction of BTB integrity and the apoptosis of spermatogenic cells through the activation of MAPK-Nrf2 pathway. The current study provided novelty evidence for elucidating the effects of PS-MPs on male reproductive toxicity and its potential mechanism.

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