Resveratrol attenuates hydrogen peroxide- and ADP-ribose-associated calcium dysregulation, oxidative stress, and apoptosis in TRPM2-transfected Chinese hamster ovary (CHO)-K1 cells.

Oxidative stress can couple reactive oxygen species generation to dysregulated intracellular calcium signaling and apoptosis. This study investigated whether resveratrol modified hydrogen peroxide (H₂O₂)- and adenosine diphosphate ribose (ADPR)-associated cellular injury in transient receptor potential melastatin 2 (TRPM2)-transfected Chinese hamster ovary (CHO)-K1 cells. Cells were assigned to control, resveratrol, H₂O₂, ADPR, H₂O₂ plus resveratrol, and ADPR plus resveratrol groups. H₂O₂ and ADPR increased the integrated Ca²⁺ response, apoptosis, JC-1 fluorescence, caspase activities, intracellular oxidant production, and malondialdehyde, but reduced glutathione and glutathione peroxidase activity (p < 0.05). Resveratrol pretreatment attenuated most of these effects and restored the glutathione and glutathione peroxidase-related antioxidant indices; however, it did not decrease malondialdehyde under the tested conditions, a dissociation that is compatible with the different temporal resolution of the two oxidant readouts used here. These findings indicate that resveratrol modifies several oxidative, calcium-associated, mitochondrial, and apoptotic responses in TRPM2-transfected CHO-K1 cells.