Oxidative Stress Responses and Gene Transcription of Mice under Chronic-Exposure to 2,6-Dichlorobenzoquinone

Int J Environ Res Public Health. 2022 Oct 24;19(21):13801. doi: 10.3390/ijerph192113801.

Abstract

2,6-Dichlorobenzoquinone (2,6-DCBQ), as an emerging disinfection by-production, was frequently detected and identified in the drinking water; however, limited information is available for the toxic effect of 2,6-DCBQ on mice. In the present study, adult mice were used to assess the impact of 2,6-DCBQ via measuring the responses of antioxidant enzymes (superoxide dismutase (SOD) and catalase (CAT)), the key genes (Heme oxygenase-1 (HO-1), NADPH quinone oxidoreductase 1 (NQO1) and glutamate-L-cysteine ligase catalytic subunit (GCLC)) in the Nrf2-keap1 pathway, and lipid peroxidation (malonaldehyde, MDA). Our results clearly indicated that 2,6-DCBQ decreased the activities of SOD and CAT, repressed the transcriptional levels of key genes in Nrf2-keap1 pathway, further caused oxidative damage on mice. These results provided evidence for assessing the threat of 2,6-DCBQ on human.

Keywords: 2,6-dichlorobenzoquinone; Nrf2-keap1; lipid peroxidation; mRNA transcription; mouse; oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / metabolism
  • Humans
  • Kelch-Like ECH-Associated Protein 1 / genetics
  • Kelch-Like ECH-Associated Protein 1 / metabolism
  • Mice
  • NF-E2-Related Factor 2* / genetics
  • Oxidative Stress*
  • Superoxide Dismutase / metabolism
  • Transcription, Genetic

Substances

  • Kelch-Like ECH-Associated Protein 1
  • NF-E2-Related Factor 2
  • 2,6-dichlorobenzoquinone
  • Antioxidants
  • Superoxide Dismutase

Grants and funding

This work was supported by the National Nature Science Foundation of China (grants 21707123, 41907118, 41771524), the Basic Public Welfare Research Project in Zhejiang Province (grants LGF19B070007).