Pharmacological doses of melatonin induce alterations in mitochondrial mass and potential, bcl-2 levels and K+ currents in UVB-exposed U937 cells.

摘要: Apoptosis is observed in 'actively' dying cells after the exposure to cell stressors such as ultraviolet light irradiation. Since melatonin has been proposed act under stressful conditions protection factor, this study we examined potential of molecule when used at pharmacological concentrations control mitochondrial damage and apoptotic signalling UVB irradiated U937 human leukaemic cells. Moreover, effect treatment on electrophysiological properties membrane K(+) currents was investigated functional aspects relevant anti-apoptotic role melatonin. The general associated with restoration mass, number mitochondria, a lower caspase activation bcl-2 upregulation. In presence inhibitor ZVAD-Fmk, seems drive stressed follow intrinsic pathway, interfering just level. melatonin, well prevented current reduction late following insult application, by sparing from death; result also indicates that decrease leakage could represent feature process UV-exposed