2. Academic Validation
  3. 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: [email protected].
  • 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.
PMID: 37327611 DOI: 10.1016/j.jhazmat.2023.131840
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.

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