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A protective action of melatonin (MELAT) on docetaxel (DCT)-induced inflammation, apoptosis, and reactive free oxygen radical (fROS) generation values via blocking of TRPM2 calcium-permeable channel was investigated in different cells except for laryngo-tracheal epithelial (LT-Epi) cells. Hence, the protective action of MELAT on DCT-induced oxidative toxicity and inflammation in LT-Epi tissue and cells of mice were investigated in the current study. MELAT treatment ameliorated DCT-induced mitochondrial ROS in the LT-Epi cells by reducing the generation of fROS (cytosolic and mitochondrial), lipid peroxidation, and depolarization of the mitochondrial membrane, while increasing reduced glutathione (GSH), GSH peroxidase, and total antioxidant status. In addition, DCT-induced increases of cytokine (IL-1β, IL-6, and TNF-α) generations were also diminished in the LT-Epi tissue by MELAT treatment. Furthermore, MELAT treatment increased viability and count of the cells followed by decreasing levels of cell death, caspase -3, and -9. The TRPM2 activity was also reduced by MELAT and TRPM2 channel blocker (ACA) treatments. In conclusion, MELAT modulated the increase of DCT-induced LT-Epi cell death by inhibiting mitochondrial oxidative stress and TRPM2 channel activity. Hence, DCT-caused side cell death, oxidant, and inflammatory actions in the LT-Epi were diminished via the treatment of MELAT.

Melatonin ameliorates docetaxel-induced mitochondrial oxidative toxicity and cytokine generation in the laryngo-tracheal epithelial cell