Mitochondrial ROS production, oxidative stress and aging within and between species: Evidences and recent advances on this aging effector

Mitochondria play a wide diversity of roles in cell physiology and have a key functional implication in cell bioenergetics and biology of free radicals. As the main cellular source of oxygen radicals, mitochondria have been postulated as the mediators of the cellular decline associated with the biol...

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Detalles Bibliográficos
Autores: Gómez, José, Mota Martorell, Natàlia, Jové Font, Mariona, Pamplona Gras, Reinald, Barja, Gustavo
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2023
País:España
Institución:Universitat de Lleida (UdL)
Repositorio:Repositori Obert UdL
OAI Identifier:oai:repositori.udl.cat:10459.1/464305
Acceso en línea:https://doi.org/10.1016/j.exger.2023.112134
https://hdl.handle.net/10459.1/464305
Access Level:acceso abierto
Palabra clave:Animal longevity
Complex I
DNA damage
DNA fragments
Electron transport chain
NDUFV2 subuni
Descripción
Sumario:Mitochondria play a wide diversity of roles in cell physiology and have a key functional implication in cell bioenergetics and biology of free radicals. As the main cellular source of oxygen radicals, mitochondria have been postulated as the mediators of the cellular decline associated with the biological aging. Recent evidences have shown that mitochondrial free radical production is a highly regulated mechanism contributing to the biological determination of longevity which is species-specific. This mitochondrial free radical generation rate induces a diversity of adaptive responses and derived molecular damage to cell components, highlighting mitochondrial DNA damage, with biological consequences that influence the rate of aging of a given animal species. In this review, we explore the idea that mitochondria play a fundamental role in the determination of animal longevity. Once the basic mechanisms are discerned, molecular approaches to counter aging may be designed and developed to prevent or reverse functional decline, and to modify longevity.