Melatonin reduces pancreatic tumor cell viability by altering mitochondrial physiology.

Antonio Gonzalez, Angel del Castillo-Vaquero, Alvaro Miro-Moran, Jose A Tapia, Gines M Salido

Department of Physiology, Cell Physiology Research Group, University of Extremadura, Caceres, Spain. agmateos@unex.es

Journal of pineal research 2011 Apr

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Melatonin reduces proliferation in many different cancer cell lines. Thus, melatonin is considered a promising antitumor agent, promoting apoptosis in tumor cells while preserving viability of normal cells. Herein, we examined the effects of melatonin on the pancreatic AR42J tumor cell line. We have analyzed cytosolic-free Ca(2+) concentration ([Ca(2+) ](c) ), mitochondrial-free Ca(2+) concentration ([Ca(2+) ](m) ), mitochondrial membrane potential (Ψm), mitochondrial flavin adenine dinucleotide (FAD) oxidative state, cellular viability and caspase-3 activity. Our results show that melatonin induced transient changes in [Ca(2+) ](c) and [Ca(2+) ](m) . Melatonin also induced depolarization of Ψm and led to a reduction in the level of oxidized FAD. In addition, melatonin reduced AR42J cell viability. Finally, we found a Ca(2+) -dependent caspase-3 activation in response to melatonin. Collectively, these data support the likelihood that melatonin reduces viability of tumor AR42J cells via its action on mitochondrial activity and caspase-3 activation. © 2010 The Authors. Journal of Pineal Research © 2010 John Wiley & Sons A/S.

Citation

Antonio Gonzalez, Angel del Castillo-Vaquero, Alvaro Miro-Moran, Jose A Tapia, Gines M Salido. Melatonin reduces pancreatic tumor cell viability by altering mitochondrial physiology. Journal of pineal research. 2011 Apr;50(3):250-60