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Activation of TRPM8 channel through oxidative stress may induce Ca 2+  and pro-apoptotic signals in prostate cancer and kidney cells. The aim of this study was to evaluate activation of TRPM8 can increase apoptosis and oxidative stress in the prostate cancer (Du145 M8 ), TRPM8 knock out (Du 145 M8KO ), transfected (HEK293 TM8 ) and non-transfected human kidney (HEK293) cells. Intracellular Ca 2+  responses to TRPM8 activation were increased in the Du145 M8  and HEK293 TM8  cells from coming cumene hydrogen peroxide (CHPx), menthol, ADP-Ribose (ADPR), but not in the HEK293 and Du 145 M8KO  cells. The intracellular Ca 2+  responses to both ADPR and CHPx were totally inhibited by the thiol cycle antioxidant glutathione, and TRPM8 blockers (N-(p-amylcinnamoyl)anthranilic acid and capsazepine). Apoptosis, Annexin V, mitochondrial membrane depolarization, intracellular ROS, caspase 3 and 9 values were increased through TRPM8 activation in the Du 145 M8  but not in the Du 145 M8KO  and non-transfected HEK293 cells by CHPx and hydrogen peroxide. In conclusion, apoptotic and oxidant effects on the cells were increased activation of TRPM8 by oxidative stress and ADPR. Activation of TRPM8 through oxidative stress and ADPR in the cells could be used as an effective strategy in the treatment of prostate cancer cells.

ADP-Ribose and oxidative stress activate TRPM8 channel in prostate cancer and kidney cells