Aging, free radicals and antioxidants

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The article presents aging as a multifactorial, progressive biological process shaped by intersecting theories, with special focus on oxidative stress and free radical involvement. The Free Radical Theory of Aging posits that reactive oxygen species (ROS), produced both endogenously and via environm...

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Detalles Bibliográficos
Autores: Eduardo Menéndez-Álvarez, Edmme Baguer
Formato: artículo
Fecha de Publicación:2025
Institución:Universidad Le Cordon Bleu
Repositorio:Revistas - Universidad Le Cordon Bleu
Lenguaje:español
OAI Identifier:oai:ojs2.172.177.98.34:article/370
Enlace del recurso:https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370
Nivel de acceso:acceso abierto
Materia:Daño celular
estrés oxidativo
homeostasis
longevidad
peroxidación lipídicaperoxidación lipídica
Cellular damage
oxidative stress
longevity
lipid peroxidation
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spelling Aging, free radicals and antioxidantsEnvejecimiento, radicales libres y antioxidantesEduardo Menéndez-ÁlvarezEdmme BaguerDaño celularestrés oxidativohomeostasislongevidadperoxidación lipídicaperoxidación lipídicaCellular damageoxidative stresshomeostasislongevitylipid peroxidationThe article presents aging as a multifactorial, progressive biological process shaped by intersecting theories, with special focus on oxidative stress and free radical involvement. The Free Radical Theory of Aging posits that reactive oxygen species (ROS), produced both endogenously and via environmental exposures, induce cumulative molecular damage to lipids, proteins, and DNA impacting cellular and tissue integrity. This oxidative stress contributes to age-related degenerative diseases such as cancer and Alzheimer’s. Although antioxidants (both endogenous enzymes and exogenous dietary compounds) offer protective mechanisms against ROS, empirical evidence on their efficacy in extending lifespan remains inconclusive, largely due to bioavailability challenges and systemic complexity. The article also addresses mitochondrial dysfunction and genomic instability especially mitochondrial DNA mutations as key contributors to aging, proposing a dynamic interaction between genetic regulation, oxidative insults, and physiological decline. Experimental findings from animal models suggest associations between oxidative damage and aging phenotypes, though not always consistent across species. The authors advocate for a comprehensive approach that integrates molecular, genetic, and environmental perspectives, urging evidence based public health strategies to manage the rising aging population. In sum, aging is characterized as a heterogeneous, irreversible process not reducible to a single cause but rather to a complex network of biological mechanisms.En el artículo se examina el envejecimiento como un proceso biológico multifactorial, intrínseco y progresivo, vinculado a múltiples teorías complementarias. Se destaca el rol central de las especies reactivas de oxígeno (ROS), particularmente los radicales libres, como agentes prooxidantes que generan daño molecular acumulativo en lípidos, proteínas y ADN, promoviendo disfunción celular y organular. La teoría del estrés oxidativo, propuesta por Denham Harman, sugiere que el desequilibrio entre prooxidantes y antioxidantes conduce a la peroxidación lipídica, mutaciones somáticas y senescencia celular. Aunque se han investigado estrategias terapéuticas basadas en antioxidantes endógenos y exógenos (enzimáticos y no enzimáticos), los resultados in vivo sobre longevidad y prevención de enfermedades asociadas han sido inconsistentes, posiblemente debido a la baja biodisponibilidad y efectos pleiotrópicos. Se revisan teorías genéticas como la del “reloj biológico”, junto con la contribución mitocondrial al envejecimiento a través de la disfunción en la cadena de transporte de electrones y acumulación de daño en el ADNmt. El trabajo resalta la necesidad de un enfoque integrador que vincule modelos genéticos, moleculares y ambientales, así como la urgencia de establecer políticas de salud pública basadas en evidencia para abordar el aumento en la población adulta mayor.Universidad Le Cordon Bleu2025-01-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdftext/htmltext/xmlhttps://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/37010.36955/RIULCB.2025v12n1.005Revista de Investigaciones de la Universidad Le Cordon Bleu; Vol. 12 Núm. 1 (2025): ; 55 - 672409-1537reponame:Revistas - Universidad Le Cordon Bleuinstname:Universidad Le Cordon Bleuinstacron:ULCBspahttps://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370/648https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370/660https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370/667Derechos de autor 2025 Revista de Investigaciones de la Universidad Le Cordon Bleuinfo:eu-repo/semantics/openAccessoai:ojs2.172.177.98.34:article/3702025-09-08T16:19:26Z
dc.title.none.fl_str_mv Aging, free radicals and antioxidants
Envejecimiento, radicales libres y antioxidantes
title Aging, free radicals and antioxidants
spellingShingle Aging, free radicals and antioxidants
Eduardo Menéndez-Álvarez
Daño celular
estrés oxidativo
homeostasis
longevidad
peroxidación lipídicaperoxidación lipídica
Cellular damage
oxidative stress
homeostasis
longevity
lipid peroxidation
title_short Aging, free radicals and antioxidants
title_full Aging, free radicals and antioxidants
title_fullStr Aging, free radicals and antioxidants
title_full_unstemmed Aging, free radicals and antioxidants
title_sort Aging, free radicals and antioxidants
dc.creator.none.fl_str_mv Eduardo Menéndez-Álvarez
Edmme Baguer
author Eduardo Menéndez-Álvarez
author_facet Eduardo Menéndez-Álvarez
Edmme Baguer
author_role author
author2 Edmme Baguer
author2_role author
dc.subject.none.fl_str_mv Daño celular
estrés oxidativo
homeostasis
longevidad
peroxidación lipídicaperoxidación lipídica
Cellular damage
oxidative stress
homeostasis
longevity
lipid peroxidation
topic Daño celular
estrés oxidativo
homeostasis
longevidad
peroxidación lipídicaperoxidación lipídica
Cellular damage
oxidative stress
homeostasis
longevity
lipid peroxidation
description The article presents aging as a multifactorial, progressive biological process shaped by intersecting theories, with special focus on oxidative stress and free radical involvement. The Free Radical Theory of Aging posits that reactive oxygen species (ROS), produced both endogenously and via environmental exposures, induce cumulative molecular damage to lipids, proteins, and DNA impacting cellular and tissue integrity. This oxidative stress contributes to age-related degenerative diseases such as cancer and Alzheimer’s. Although antioxidants (both endogenous enzymes and exogenous dietary compounds) offer protective mechanisms against ROS, empirical evidence on their efficacy in extending lifespan remains inconclusive, largely due to bioavailability challenges and systemic complexity. The article also addresses mitochondrial dysfunction and genomic instability especially mitochondrial DNA mutations as key contributors to aging, proposing a dynamic interaction between genetic regulation, oxidative insults, and physiological decline. Experimental findings from animal models suggest associations between oxidative damage and aging phenotypes, though not always consistent across species. The authors advocate for a comprehensive approach that integrates molecular, genetic, and environmental perspectives, urging evidence based public health strategies to manage the rising aging population. In sum, aging is characterized as a heterogeneous, irreversible process not reducible to a single cause but rather to a complex network of biological mechanisms.
publishDate 2025
dc.date.none.fl_str_mv 2025-01-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370
10.36955/RIULCB.2025v12n1.005
url https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370
identifier_str_mv 10.36955/RIULCB.2025v12n1.005
dc.language.none.fl_str_mv spa
language spa
dc.relation.none.fl_str_mv https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370/648
https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370/660
https://revistas.ulcb.edu.pe/index.php/REVISTAULCB/article/view/370/667
dc.rights.none.fl_str_mv Derechos de autor 2025 Revista de Investigaciones de la Universidad Le Cordon Bleu
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Derechos de autor 2025 Revista de Investigaciones de la Universidad Le Cordon Bleu
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
text/html
text/xml
dc.publisher.none.fl_str_mv Universidad Le Cordon Bleu
publisher.none.fl_str_mv Universidad Le Cordon Bleu
dc.source.none.fl_str_mv Revista de Investigaciones de la Universidad Le Cordon Bleu; Vol. 12 Núm. 1 (2025): ; 55 - 67
2409-1537
reponame:Revistas - Universidad Le Cordon Bleu
instname:Universidad Le Cordon Bleu
instacron:ULCB
instname_str Universidad Le Cordon Bleu
instacron_str ULCB
institution ULCB
reponame_str Revistas - Universidad Le Cordon Bleu
collection Revistas - Universidad Le Cordon Bleu
repository.name.fl_str_mv
repository.mail.fl_str_mv
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