El profesor Russel J. Reiter (USA) impartirá una de las conferencias magistrales del II Congreso Intercontinental de Medicina Antienvejecimiento y Medicina Estética, titulada: “Mechanisms by which melatonin may inhibit age-related cancers”. Ésta se impartirá el sábado, 8 de febrero, a las 12:30 horas.


The presence of melatonin in mitochondria, either synthesized de novo in this organelle or taken up from the circulation, is instrumental in reprogramming cancer cell glucose metabolism from the cytosol (the Warburg effect) to the mitochondria in aged-related solid tumors (for example, breast cancer). Melatonin predictably achieves this action by inhibiting pyruvate dehydrogenase kinase (PDK) allowing for the upregulation of pyruvate dehydrogenase complex, which catalyzes the conversion of pyruvate to acetyl coenzyme A (acetyl CoA). Acetyl CoA feeds the citric acid cycle and increases ATP production via oxidation phosphorylation. Acetyl CoA also is required for the rate-limiting enzyme in melatonin production, arylalkylamine N-acetyltransferase (AANAT), which is in mitochondria to convert serotonin to N-acetylserotonin. This ensures melatonin production in the mitochondria of both normal cells and cancer cells. Cytosolic glycolysis is characteristic of many solid tumors that develop in the aged and enhances their ability to rapidly proliferate, to avoid apoptosis and to become metastatic. By redirecting glucose metabolism from the cytosol to the mitochondria in cancer cells, melatonin reduces tumor cell growth, subjects them to higher levels of oxidative stress and increases apoptotic cell death. Tumors in aged individuals typically appear when the endogenous melatonin levels have dropped substantially. Considering the numerous anti-cancer actions of melatonin, the implication is that the regular use of melatonin by the aging population may reduce the appearance of some types of age-related tumors.



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