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Oxidative stress and lipid peroxidation with exposure of emerging disinfection byproduct 2,6-dichlorobenzoquinone in mice
Summary
Mice exposed to 2,6-dichlorobenzoquinone, a disinfection byproduct found in drinking water, experienced oxidative stress and lipid damage in the liver and kidneys. Disinfection byproducts can form when chlorine reacts with organic matter in water, including chemicals leached from plastics, raising concerns about combined exposures in tap water.
Abstract 2,6-dichlorobenzoquinone (2,6-DCBQ) is an emerging disinfection byproduct frequently detected in drinking water. Previous studies have indicated that 2,6-DCBQ causes oxidative stress damage in some live systems, but this has yet to be tested in vivo in mammals. In the present study, adult mice were exposed to 2,6-DCBQ for 30 d via gavage at 0 ~ 100 mg kg − 1 with the responses of antioxidant enzymes (superoxide dismutase [SOD] and catalase [CAT]), key oxidative stress response 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) as an indicator of oxidative damage being measured. Our results indicated that 2,6-DCBQ decreased the activities of SOD and CAT, repressed transcription of key genes in the Nrf2-keap1 pathway, and caused measurable oxidative damage. These results reveal the impact of 2,6-DCBQ in a model mammalian system and are key to understanding the potential impacts of 2,6-DCBQ in humans.
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