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暴露于聚苯乙烯微塑料会通过氧化应激和激活 p38 MAPK 信号通路引起生殖毒性。

Exposure to polystyrene microplastics causes reproductive toxicity through oxidative stress and activation of the p38 MAPK signaling pathway.

机构信息

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, Hubei, 430079, China.

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, Hubei, 430079, China.

出版信息

Ecotoxicol Environ Saf. 2020 Mar 1;190:110133. doi: 10.1016/j.ecoenv.2019.110133. Epub 2019 Dec 30.

Abstract

Microplastics (MP) are receiving increased attention as a harmful environmental pollutant, however information on the reproduction toxicity of MP in terrestrial animals, especially mammals, is limited. In this experiment, we investigated the impact of polystyrene microplastics (micro-PS) on the reproductive system of male mice. Healthy Balb/c mice were exposed to saline or to different doses of micro-PS for 6 weeks. The results showed that micro-PS exposure resulted in a significant decrease in the number and motility of sperm, and a significant increase in sperm deformity rate. We also detected a decrease in the activity of the sperm metabolism-related enzymes, succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), and a decrease in the serum testosterone content in the micro-PS exposure group. We found that micro-PS exposure caused oxidative stress and activated JNK and p38 MAPK. In addition, we found that when N-acetylcysteine (NAC) scavenges ROS, and when the p38 MAPK-specific inhibitor SB203580 inhibits p38MAPK, the micro-PS-induced sperm damage is alleviated and testosterone secretion improves. In conclusion, our findings suggest that micro-PS induces reproductive toxicity in mice through oxidative stress and activation of the p38 MAPK signaling pathways.

摘要

微塑料(MP)作为一种有害的环境污染物,受到了越来越多的关注,然而,关于 MP 对陆生动物,特别是哺乳动物的生殖毒性的信息有限。在本实验中,我们研究了聚苯乙烯微塑料(微 PS)对雄性小鼠生殖系统的影响。将健康的 Balb/c 小鼠暴露于生理盐水或不同剂量的微 PS 中 6 周。结果表明,微 PS 暴露导致精子数量和活力显著下降,精子畸形率显著升高。我们还检测到精子代谢相关酶琥珀酸脱氢酶(SDH)和乳酸脱氢酶(LDH)的活性降低,以及微 PS 暴露组血清睾酮含量降低。我们发现微 PS 暴露引起氧化应激并激活 JNK 和 p38 MAPK。此外,我们发现当 N-乙酰半胱氨酸(NAC)清除 ROS 时,当 p38 MAPK 特异性抑制剂 SB203580 抑制 p38MAPK 时,微 PS 诱导的精子损伤减轻,睾酮分泌改善。总之,我们的研究结果表明,微 PS 通过氧化应激和激活 p38 MAPK 信号通路诱导小鼠生殖毒性。

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