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dc.contributor.author
Reiter, Russel
dc.contributor.author
Sharma, Ramaswamy
dc.contributor.author
Rosales Corral, Sergio
dc.contributor.author
Manucha, Walter Ariel Fernando
dc.contributor.author
Almeida Chuffa, Luiz Gustavo de
dc.contributor.author
Pires de Campos Zuccari, Debora Aparecida
dc.date.available
2022-10-14T16:03:15Z
dc.date.issued
2021-11
dc.identifier.citation
Reiter, Russel; Sharma, Ramaswamy; Rosales Corral, Sergio; Manucha, Walter Ariel Fernando; Almeida Chuffa, Luiz Gustavo de; et al.; Melatonin and pathological cell interactions: mitochondrial glucose processing in cancer cells; Multidisciplinary Digital Publishing Institute; International Journal of Molecular Sciences; 22; 22; 11-2021; 1-22
dc.identifier.issn
1422-0067
dc.identifier.uri
http://hdl.handle.net/11336/173275
dc.description.abstract
Melatonin is synthesized in the pineal gland at night. Since melatonin is produced in the mitochondria of all other cells in a non-circadian manner, the amount synthesized by the pineal gland is less than 5% of the total. Melatonin produced in mitochondria influences glucose metabolism in all cells. Many pathological cells adopt aerobic glycolysis (Warburg effect) in which pyruvate is excluded from the mitochondria and remains in the cytosol where it is metabolized to lactate. The entrance of pyruvate into the mitochondria of healthy cells allows it to be irreversibly decarboxylated by pyruvate dehydrogenase (PDH) to acetyl coenzyme A (acetyl-CoA). The exclusion of pyruvate from the mitochondria in pathological cells prevents the generation of acetyl-CoA from pyruvate. This is relevant to mitochondrial melatonin production, as acetyl-CoA is a required co-substrate/co-factor for melatonin synthesis. When PDH is inhibited during aerobic glycolysis or during intracellular hypoxia, the deficiency of acetyl-CoA likely prevents mitochondrial melatonin synthesis. When cells experiencing aerobic glycolysis or hypoxia with a diminished level of acetyl-CoA are supplemented with melatonin or receive it from another endogenous source (pineal-derived), pathological cells convert to a more normal phenotype and support the transport of pyruvate into the mitochondria, thereby re-establishing a healthier mitochondrial metabolic physiology.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Multidisciplinary Digital Publishing Institute
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by/2.5/ar/
dc.subject
AEROBIC GLYCOLYSIS
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CANCER
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DISEASED CELLS
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MELATONIN
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MITOCHONDRIAL METABOLISM
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WARBURG EFFECT
dc.subject.classification
Otras Ciencias de la Salud
dc.subject.classification
Ciencias de la Salud
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Melatonin and pathological cell interactions: mitochondrial glucose processing in cancer cells
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2022-09-20T18:02:55Z
dc.journal.volume
22
dc.journal.number
22
dc.journal.pagination
1-22
dc.journal.pais
Suiza
dc.journal.ciudad
Basilea
dc.description.fil
Fil: Reiter, Russel. University Of Texas At San Antonio. University Of Texas Health Science Center At San Antonio (ut Health San Antonio); Estados Unidos
dc.description.fil
Fil: Sharma, Ramaswamy. University Of Texas At San Antonio. University Of Texas Health Science Center At San Antonio (ut Health San Antonio); Estados Unidos
dc.description.fil
Fil: Rosales Corral, Sergio. Instituto Mexicano del Seguro Social; México
dc.description.fil
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
dc.description.fil
Fil: Almeida Chuffa, Luiz Gustavo de. Institute of Biosciences of Botucatu; Brasil
dc.description.fil
Fil: Pires de Campos Zuccari, Debora Aparecida. Faculdade de Medicina de Sao Jose Do Rio Preto; Brasil
dc.journal.title
International Journal of Molecular Sciences
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/22/22/12494
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.3390/ijms222212494
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