Threats of nano/microplastics to reproduction and offspring: Potential mechanisms and perspectives

Mei Ha; Wanzhen Tang; Jichun Huang; Changjiang Liu

doi:10.59400/jts.v2i1.443

Mei Ha School of Nursing, Chongqing Medical and Pharmaceutical College, Chongqing 401331, China
Wanzhen Tang School of Nursing, Chongqing Medical and Pharmaceutical College, Chongqing 401331, China
Jichun Huang School of Nursing, Chongqing Medical and Pharmaceutical College, Chongqing 401331, China
Changjiang Liu NHC Key Laboratory of Birth Defects and Reproductive Health, Chongqing Population and Family Planning Science and Technology Research Institute, Chongqing 401120, China

Article ID: 443

177 Views, 99 PDF Downloads

DOI: https://doi.org/10.59400/jts.v2i1.443

Keywords: nano/microplastics; reproduction; offspring; adverse effects

Abstract

Due to their ubiquitous occurrence in the aquatic environment and terrestrial ecosystem and underlying eco-environmental risks, nano/microplastics (NPs/MPs) have sparked great public concerns. The purpose of this work is aimed to summarize the harmful influence of NPs/MPs on reproduction and offspring health and further explore the potential mechanisms of action, thereby facilitating the more comprehensive understanding of NPs/MPs features. Literature search databases included EMBASE, Web of Science, and PubMed. The study selection and data extraction were implemented according to the inclusion criteria. NPs/MPs could accumulate and trigger reproductive toxic responses and thereafter generate deleterious effects on the offspring's health. Accordingly, the reproductive toxicity of NPs/MPs was characterized as the sperm deformity, decline in sperm count and motility, follicular growth tardiness, ovarian fibrosis, granulosa cell death, disorder of reproductive hormone secretion, as well as the fetal growth restriction, glycolipid metabolism disorder, and inflammatory responses of the next generation. Additionally, mechanism research revealed that NPs/MPs exposure brought about inflammatory responses and oxidative stress and thereafter destroyed the blood-testis barrier (BTB) integrity, motivated spermatogenic cell apoptosis by activating the JNK and p38/MAPK-Nrf2/NF-κB pathways, and induced ovarian granulosa cell pyroptosis and apoptosis and subsequent ovarian fibrosis via the Wnt/β-Catenin and NLRP3/Caspase-1 pathways. Nevertheless, this work also highlighted the imperative requirements for scientific and systematic risk assessments of NPs/MPs, so as to identify feasible risk mitigation strategies.

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