1. Academic Validation
  2. SKN-1/Nrf2-dependent regulation of mitochondrial homeostasis modulates transgenerational toxicity induced by nanoplastics with different surface charges in Caenorhabditis elegans

SKN-1/Nrf2-dependent regulation of mitochondrial homeostasis modulates transgenerational toxicity induced by nanoplastics with different surface charges in Caenorhabditis elegans

  • J Hazard Mater. 2023 Jun 13;457:131840. doi: 10.1016/j.jhazmat.2023.131840.
Man Qu 1 Long Miao 2 He Chen 3 Xing Zhang 4 Yang Wang 5
Affiliations

Affiliations

  • 1 School of Public Health, Yangzhou University, Yangzhou 225000, China. Electronic address: man.qu@yzu.edu.cn.
  • 2 School of Public Health, Yangzhou University, Yangzhou 225000, China.
  • 3 Institutes of Physical Science and Information Technology, Anhui University, Hefei 230000, China.
  • 4 The State Key Laboratory of Translational Medicine and Innovative Drug Development, Jiangsu Simcere Diagnostics Co., Ltd., Nanjing 210009, China.
  • 5 Yangzhou Hospital of Traditional Chinese Medicine Affiliated to the School of Clinical Chinese Medicine, Yangzhou University, Yangzhou 225000, China.
Abstract

The toxic effects of nanoplastics on transgenerational toxicity in environmental organisms and the involved mechanisms remain poorly comprehended. This study aimed to identify the role of SKN-1/Nrf2-dependent regulation of mitochondrial homeostasis in response to transgenerational toxicity caused by changes in nanoplastic surface charges in Caenorhabditis elegans (C. elegans). Our results revealed that compared with the wild-type control and PS exposed groups, exposure to PS-NH2 or PS-SOOOH at environmentally relevant concentrations (ERC) of ≥ 1 μg/L caused transgenerational reproductive toxicity, inhibited mitochondrial unfolded protein responses (UPR) by downregulating the transcription levels of hsp-6, ubl-5, dve-1, atfs-1, haf-1, and clpp-1, membrane potential by downregulating phb-1 and phb-2, and promoted mitochondrial Apoptosis by downregulating ced-4 and ced-3 and upregulating ced-9, DNA damage by upregulating hus-1, cep-1, egl-1, Reactive Oxygen Species (ROS) by upregulating nduf-7 and nuo-6, ultimately resulting in mitochondrial homeostasis. Additionally, further study indicated that SKN-1/Nrf2 mediated antioxidant response to alleviate PS-induced toxicity in the P0 generation and dysregulated mitochondrial homeostasis to enhance PS-NH2 or PS-SOOOH-induced transgenerational toxicity. Our study highlights the momentous role of SKN-1/Nrf2 mediated mitochondrial homeostasis in the response to nanoplastics caused transgenerational toxicity in environmental organisms.

Keywords

Mitochondrial homeostasis; Nanoplastics; SKN-1/Nrf2; Surface charge; Transgenerational toxicity.

Figures
Products