Melatonin and Its Metabolites Ameliorate UVR-Induced Mitochondrial Oxidative Stress in Human MNT-1 Melanoma Cells.

摘要: Melatonin (Mel) is the major biologically active molecule secreted by pineal gland. Mel and its metabolites, 6-hydroxymelatonin (6(OH)Mel) 5-methoxytryptamine (5-MT), possess a variety of functions, including scavenging free radicals induction protective or reparative mechanisms in cell. Their amphiphilic character allows them to cross cellular membranes reach subcellular organelles, mitochondria. Herein, action Mel, 6(OH)Mel, 5-MT human MNT-1 melanoma cells against ultraviolet B (UVB) radiation was investigated. The dose 50 mJ/cm² caused significant reduction cell viability up 48%, while investigated compounds counteracted this deleterious effect. UVB exposure increased catalase activity led simultaneous Ca++ influx (16%), tested prevented these disturbances. Additional analysis focused on mitochondrial respiration performed isolated mitochondria from liver BALB/cJ mice where significantly enhanced oxidative phosphorylation at 10-6 M with lower effects seen 10-9 10-4 M. In conclusion, 6(OH)Mel protect cells, which express melatonin receptors (MT1 MT2) UVB-induced stress dysfunction, uncoupling phosphorylation.