0
Article ? AI-assigned paper type based on the abstract. Classification may not be perfect — flag errors using the feedback button. Tier 2 ? Original research — experimental, observational, or case-control study. Direct primary evidence. Human Health Effects Reproductive & Development Sign in to save

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

Ecotoxicology and Environmental Safety 2019 580 citations ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Xiaoman Xie, Ting Deng, Jiufei Duan, Jing Xie, Junlin Yuan, Mingqing Chen

Summary

Researchers exposed male mice to polystyrene microplastics for six weeks and observed significant reproductive harm, including decreased sperm count, reduced motility, and increased deformity rates. The damage was linked to oxidative stress and activation of a specific cellular signaling pathway called p38 MAPK. The findings suggest that microplastic exposure may pose risks to male reproductive health in mammals through oxidative stress mechanisms.

Polymers
Body Systems
Models

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.

Share this paper