Response pathways of superoxide dismutase and catalase under the regulation of triclocarban-triggered oxidative stress in Eisenia foetida: Comprehensive mechanism analysis based on cytotoxicity and binding model.

Triclocarban (TCC) is an emerging environmental contaminant, posing potential ecological risks. Displaying a high accumulation effect and 120-day half-life in the soil environment, the toxic effects of TCC to soil organisms have been widely reported. Previous studies have confirmed that TCC can induce the oxidative stress and changes in superoxide dismutase (SOD) and catalase (CAT) activities in earthworms, but the underlying mechanisms of oxidative stress and disorder in antioxidant enzyme activities induced by TCC have not yet been elucidated. Here, we explored the multiple response mechanisms of SOD and CAT under the regulation of oxidative stress induced by TCC. Results indicated that higher-dose (0-2.0 mg/L) TCC exposure triggered the overproduction of ROS in Eisenia foetida coelomocytes, causing oxidative damage and a decrease in cell viability that was response to ROS accumulation. The TCC-induced inhibition of intracellular SOD/CAT activity was found under the regulation of oxidative stress (SOD: 29.2 %; CAT: 18.5 %), and this effect was blunted by antioxidant melatonin. At the same time, the interaction between antioxidative enzymes and TCC driven by various forces (SOD: electrostatic interactions; CAT: van der Waals forces and hydrogen bonding) led to inhibited SOD activity (9.84 %) and enhanced CAT activity (17.5 %). Then, to elucidate the binding mode of TCC, we explored the changes in SOD and CAT structure (protein backbone and secondary structure), the microenvironment of aromatic amino acids, and aggregation behavior through multispectral techniques. Molecular docking results showed that 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 regulation of TCC-triggered oxidative stress and shed a new light on revealing the toxic pathways of exogenous pollutants on antioxidant-related proteins function.