Response pathways of superoxide dismutase and catalase under theregulation of triclocarban-triggered oxidative stress inEisenia foetida:Comprehensive mechanism analysis based on cytotoxicity andbinding model

Triclocarban (TCC) is an emerging environmental contaminant, posing potential ecological risks. Displaying a high ac-cumulation effect and 120-day half-life in the soil environment, the toxic effects of TCC to soil organisms have beenwidely reported. Previous studies have confirmed that TCC can induce the oxidative stress and changes in superoxidedismutase (SOD) and catalase (CAT) activities in earthworms, but the underlying mechanisms of oxidative stress anddisorder in antioxidant enzyme activities induced by TCC have not yet been elucidated. Here, we explored the multipleresponse mechanisms of SOD and CAT under the regulation of oxidative stress induced by TCC. Results indicated thathigher-dose (0-2.0 mg/L) TCC exposure triggered the overproduction of ROS inEisenia foetidacoelomocytes, causingoxidative damage and a decrease in cell viability that was response to ROS accumulation. The TCC-induced inhibitionof intracellular SOD/CAT activity was found under the regulation of oxidative stress (SOD: 29.2 %; CAT: 18.5 %), andthis effect was blunted by antioxidant melatonin. At the same time, the interaction between antioxidative enzymes andTCC driven by various forces (SOD: electrostatic interactions; CAT: van der Waals forces and hydrogen bonding) led toinhibited SOD activity (9.84 %) and enhanced CAT activity (17.5 %). Then, to elucidate the binding mode of TCC, weexplored the changes in SOD and CAT structure (protein backbone and secondary structure), the microenvironment ofaromatic amino acids, and aggregation behavior through multispectral techniques. Molecular docking results showedthat TCC inhibited SOD activity in a substrate competitive manner and enhanced CAT activity by the stabilizing effects of TCC on the heme groups. Collectively, this study reveals the response mechanisms of SOD/CAT under the regulationof TCC-triggered oxidative stress and shed a new light on revealing the toxic pathways of exogenous pollutants onantioxidant-related proteins function.