College of Geography and Environmental Science, Zhejiang Normal University, Jinhua 321004, China.
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.
Int J Environ Res Public Health. 2022 Oct 24;19(21):13801. doi: 10.3390/ijerph192113801.
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.
2,6-二氯苯醌（2,6-DCBQ）作为一种新兴的消毒副产物，经常在饮用水中被检测到和识别；然而，关于 2,6-DCBQ 对小鼠的毒性作用的信息有限。在本研究中，成年小鼠被用于通过测量抗氧化酶（超氧化物歧化酶（SOD）和过氧化氢酶（CAT））、Nrf2-KEAP1 通路中的关键基因（血红素加氧酶-1（HO-1）、NADPH 醌氧化还原酶 1（NQO1）和谷氨酰胺-L-半胱氨酸连接酶催化亚基（GCLC））以及脂质过氧化（丙二醛，MDA）的反应来评估 2,6-DCBQ 的影响。我们的结果清楚地表明，2,6-DCBQ 降低了 SOD 和 CAT 的活性，抑制了 Nrf2-KEAP1 通路中关键基因的转录水平，进一步导致了小鼠的氧化损伤。这些结果为评估 2,6-DCBQ 对人类的威胁提供了证据。
