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Impacto del tabaquismo en la homeostasis redox y los niveles de 8-OHdG en pacientes con EPOC: un estudio comparativo
Osman El Jundi1, Pelin Uysal1,2, Seyma Dumur3
1Department of Chest Diseases, Faculty of Medicine, İstanbul Atlas University, Istanbul, Turkey.
BMC pulmonary medicine
|September 2, 2025
Resumen
Fumar aumenta significativamente el daño oxidativo del ADN y la peroxidación lipídica en pacientes con EPOC, lo que pone de relieve la necesidad de dejar de fumar y las terapias antioxidantes. Este estudio vincula los marcadores de estrés oxidativo más altos con la gravedad de la EPOC en los fumadores.
Área de la Ciencia:
- Medicina de los pulmones
- La bioquímica
- La genética
Sus antecedentes:
- La enfermedad pulmonar obstructiva crónica (EPOC) implica una predisposición genética y un deterioro de los sistemas antioxidantes, exacerbado por el tabaquismo.
- Fumar desencadena el estrés oxidativo, afectando el equilibrio redox celular.
- Los marcadores clave incluyen la desoxiguanosina 8-hidroxi-2' (8-OHdG) para el daño del ADN, el malondialdehído (MDA) para la peroxidación lipídica, el carbonio proteico (PCO) para el daño de las proteínas y la paraoxonasa (PON) 1 para la actividad antioxidante.
Objetivo del estudio:
- Investigar el impacto del tabaquismo en los marcadores del estrés oxidativo y la actividad antioxidante en pacientes con EPOC.
- Evaluar la relación entre el tabaquismo, el daño oxidativo y la gravedad de la EPOC.
Principales métodos:
- Un estudio transversal incluyó a 141 pacientes con EPOC (fumadores y no fumadores) y 140 controles sanos.
- Se midieron los niveles séricos de 8-OHdG, MDA, PCO y actividad PON1.
- Se realizaron correlaciones con la función pulmonar (FEV1, FEV1/ FVC) y análisis de ROC.
Principales resultados:
- Los pacientes con EPOC que fuman presentaron niveles séricos elevados de 8-OHdG, MDA y PCO, junto con una actividad PON1 reducida.
- Los niveles más altos de 8-OHdG se correlacionaron negativamente con FEV1, FEV1 / FVC y actividad PON1 en fumadores.
- El 8-OHdG mostró un fuerte poder predictivo para la EPOC en fumadores, aunque los hallazgos requieren una interpretación cautelosa debido al diseño del estudio.
Conclusiones:
- El tabaquismo exacerba el desequilibrio sistémico oxidante-antioxidante en la EPOC, deteriorando la homeostasis redox celular.
- El aumento del daño oxidativo y la reducción de la defensa antioxidante en pacientes fumadores con EPOC están relacionados con la gravedad de la enfermedad.
- El abandono del tabaco y las estrategias dirigidas a los antioxidantes son cruciales para el manejo de la EPOC.
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