Long-term exposure to polystyrene microplastics triggers premature testicular aging.

IF 7.2 1区 医学 Q1 TOXICOLOGY Particle and Fibre Toxicology Pub Date : 2023-08-28 DOI:10.1186/s12989-023-00546-6
Deyi Wu, Meng Zhang, Ting Ting Bao, Hainan Lan
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引用次数: 1

Abstract

Background: Plastic pollution is greatly serious in the ocean and soil. Microplastics (MPs) degraded from plastic has threatened animals and humans health. The accumulation of MPs in the tissues and blood in animals and humans has been found. There is therefore a need to assess the toxicological effects of MPs on the reproductive system.

Results: In this study, we explored the effect of polystyrene microplastics (PS-MPs) on premature testicular aging in vitro and in vivo. In vitro, we found that testicular sertoli cells (TM4 cells) was prematurely senescent following PS-MPs treatment by the evaluation of a range of aging marker molecules (such as Sa-β-gal, p16 and 21). TM4 cells were then employed for in vitro model to study the potential molecular mechanism by which PS-MPs induce the premature senescence of TM4 cells. NF-κB is identified as a key molecule for PS-MPs-induced TM4 cellular senescence. Furthermore, through eliminating reactive oxygen species (ROS), the activation of nuclear factor kappa B (NF-κB) was blocked in PS-MPs-induced senescent TM4 cells, indicating that ROS triggers NF-κB activation. Next, we analyzed the causes of mitochondrial ROS (mtROS) accumulation induced by PS-MPs, and results showed that Ca2+ overload induced the accumulation of mtROS. Further, PS-MPs exposure inhibits mitophagy, leading to the continuous accumulation of senescent cells. In vivo, 8-week-old C57 mice were used as models to assess the effect of PS-MPs on premature testicular aging. The results illustrated that PS-MPs exposure causes premature aging of testicular tissue by testing aging markers. Additionally, PS-MPs led to oxidative stress and inflammatory response in the testicular tissue.

Conclusion: In short, our experimental results revealed that PS-MPs-caused testicular premature aging is dependent on Ca2+/ROS/NF-κB signaling axis. The current study lays the foundation for further exploration of the effects of microplastics on testicular toxicology.

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长期接触聚苯乙烯微塑料会引发睾丸过早衰老。
背景:海洋和土壤中的塑料污染非常严重。塑料降解的微塑料已经威胁到动物和人类的健康。已经发现MP在动物和人类的组织和血液中积累。因此,有必要评估MPs对生殖系统的毒理学影响。结果:在本研究中,我们在体外和体内探索了聚苯乙烯微塑料(PS-MPs)对睾丸过早衰老的影响。在体外,我们通过评估一系列衰老标记分子(如Sa-β-gal、p16和21),发现PS-MPs治疗后睾丸支持细胞(TM4细胞)过早衰老。然后将TM4细胞用于体外模型,以研究PS-MPs诱导TM4细胞早衰的潜在分子机制。NF-κB被鉴定为PS-MPs诱导TM4细胞衰老的关键分子。此外,通过消除活性氧(ROS),核因子κB(NF-κB)的激活在PS-MPs诱导的衰老TM4细胞中被阻断,表明ROS触发NF-κB的激活。接下来,我们分析了PS-MPs诱导线粒体ROS(mtROS)积累的原因,结果表明Ca2+超载诱导了线粒体ROS的积累。此外,PS-MPs暴露抑制线粒体自噬,导致衰老细胞的持续积累。在体内,使用8周龄C57小鼠作为模型来评估PS-MPs对睾丸过早衰老的影响。通过测试衰老标志物,结果表明PS-MPs暴露会导致睾丸组织过早衰老。此外,PS-MPs导致睾丸组织中的氧化应激和炎症反应。结论:总之,我们的实验结果表明,PS-MPs引起的睾丸过早衰老依赖于Ca2+/ROS/NF-κB信号轴。目前的研究为进一步探索微塑料对睾丸毒理学的影响奠定了基础。
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来源期刊
CiteScore
15.90
自引率
4.00%
发文量
69
审稿时长
6 months
期刊介绍: Particle and Fibre Toxicology is an online journal that is open access and peer-reviewed. It covers a range of disciplines such as material science, biomaterials, and nanomedicine, focusing on the toxicological effects of particles and fibres. The journal serves as a platform for scientific debate and communication among toxicologists and scientists from different fields who work with particle and fibre materials. The main objective of the journal is to deepen our understanding of the physico-chemical properties of particles, their potential for human exposure, and the resulting biological effects. It also addresses regulatory issues related to particle exposure in workplaces and the general environment. Moreover, the journal recognizes that there are various situations where particles can pose a toxicological threat, such as the use of old materials in new applications or the introduction of new materials altogether. By encompassing all these disciplines, Particle and Fibre Toxicology provides a comprehensive source for research in this field.
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