Oxidative stress response system in Escherichia coli arising from diphenyl ditelluride (PhTe)2 exposure.

The toxicity of diphenyl ditelluride (PhTe)2 is associated with its ability to oxidize sulfhydryl groups from biological molecules. Therefore, we evaluated possible molecular mechanisms of toxicity induced by this organochalcogen in Escherichia coli (E. coli) by evaluating oxidative damage markers, relative expression of genes associated with the cellular redox state in bacteria, such as katG, sodA, sodB, soxS, and oxyR, as well as the activity of enzymes responsible for cellular redox balance. After exposure of (PhTe)2 (6, 12, and 24 μg/mL), there was a decrease in non-protein thiols (NPSH) levels, an increase in protein carbonylation and lipid peroxidation in E. coli. Intra- and extracellular reactive species (RS) was increased at concentrations of 6, 12, and 24 μg/mL. The superoxide dismutase (SOD) activity was increased at the three concentrations tested, while catalase (CAT) activity was higher at 12 and 24 μg/mL. The soxS gene showed lower expression at the three concentrations tested, while the oxyR gene was supressed at 24 μg/mL. The katG antioxidant response gene showed lower expression, and sodA and sodB were positively activated, except for sodB at 6 μg/mL. Our findings demonstrate that exposure to (PhTe)2 induced RS formation, NPSH depletion and changes in transcriptional factors regulation, characterizing it as a multi-target compound, causing disruption in cellular oxidative state, as well as molecular mechanisms associated in E. coli.