4.7 Article

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

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 28, Issue 35, Pages 47921-47931

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-021-13911-9

Keywords

Microplastics; Oxidative stress; p38 MAPK signaling pathway; Nrf2; Blood-testis barrier; Rats

Funding

  1. National Natural Science Foundation of China [81701301]
  2. Nature Science Foundation from Shanxi Province [2020JM-328]
  3. Science and Technology Innovation plan for college students in Shandong Province [S201910440051, S202010440090]

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The study found that exposure to PS-MPs led to apoptosis of spermatogenic cells, decreased sperm motility and concentration, as well as increased abnormality of sperm. Additionally, PS-MPs induced oxidative stress, activated the p38 MAPK pathway, and depleted Nrf2.
As a persistent pollutant, microplastics (MPs) have been reported to induce sperm quantity decrease in mice. 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 doses of 0 mg/day (control group), 0.015 mg/day, 0.15 mg/day, and 1.5 mg/day, respectively. The present results have shown that PS-MP exposure led to the damage of seminiferous tubule, resulted in apoptosis of spermatogenic cells, and decreased the motility and concentration of sperm, while the abnormality of sperm was elevated. Meanwhile, PS-MPs could induce oxidative stress and activate the p38 MAPK pathway and thus deplete the nuclear factor erythroid-2 related factor 2 (Nrf2). Noteworthily, PS-MPs led to the BTB-related protein expression decrease. All these results demonstrated that PS-MP exposure may lead to the destruction of BTB integrity and the apoptosis of spermatogenic cells through the activation of the 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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