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

Author

Listed:
  • Wenjing Wu

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Yingying Liu

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Chunze Li

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Fangyu Zhuo

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Zexiong Xu

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Huachang Hong

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Hongjie Sun

    (College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China)

  • Xianfeng Huang

    (National and Local Joint Engineering Research Center for Ecological Treatment Technology of Urban Water Pollution, College of Life and Environmental Science, Wenzhou University, Wenzhou 325035, China)

  • Xinwei Yu

    (Key Laboratory of Health Risk Factors for Seafood of Zhejiang Province, Zhoushan Municipal Center for Disease Control and Prevention, Zhoushan 316021, China
    College of Marine Science and Technology, Zhejiang Ocean University, Zhoushan 316021, China)

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.

Suggested Citation

  • Wenjing Wu & Yingying Liu & Chunze Li & Fangyu Zhuo & Zexiong Xu & Huachang Hong & Hongjie Sun & Xianfeng Huang & Xinwei Yu, 2022. "Oxidative Stress Responses and Gene Transcription of Mice under Chronic-Exposure to 2,6-Dichlorobenzoquinone," IJERPH, MDPI, vol. 19(21), pages 1-9, October.
    • Handle: RePEc:gam:jijerp:v:19:y:2022:i:21:p:13801-:d:951332
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