Disfunción mitocondrial y estrés oxidativo asociado al trastorno del espectro autista: Una revisión narrativa
Date
2022
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Publisher
Revista Chilena de Nutrición
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0717-7518
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Abstract
El trastorno del espectro autista (TEA) es un conjunto de alteraciones del desarrollo neurológico, deterioro de la interacción
social, lenguaje y comunicación, el cual ha aumentado a nivel mundial en los últimos años. El deterioro de esta condición
ocurre principalmente a nivel cerebral y actualmente se ha postulado que la disfunción mitocondrial (DM), el aumento del
estrés oxidativo y la disminución de la defensa antioxidante conducen a un desequilibrio en la capacidad de contrarrestar
los efectos nocivos del estrés oxidativo, como degradación oxidativa de lípidos, proteínas y ADN que puede causar daño
en el tejido cerebral, lo que conduce a síntomas clínicos y comportamientos del TEA. La disfunción mitocondrial principalmente puede ocurrir debido a anomalías en la cadena transportadora de electrones, que a su vez induce y aumenta el
estrés oxidativo. Por otro lado, el cerebro es sumamente vulnerable al estrés oxidativo, por su alto consumo de oxígeno, su
limitada capacidad antioxidante, mayor cantidad de ácidos grasos y hierro. Esta mayor susceptibilidad del cerebro al daño
oxidativo destaca la importancia de comprender el papel del estrés oxidativo en las manifestaciones clínicas del TEA. Diversos
estudios han observado un aumento de los marcadores de estrés oxidativo y una disminución en las enzimas antioxidantes
en el autismo. Por lo tanto, mejorar el estado oxidativo y mantener el equilibrio redox podría mejorar las manifestaciones
clínicas del autismo. El presente estudio tiene como objetivo realizar una revisión narrativa sobre estrés oxidativo y disfunción
mitocondrial asociado al trastorno del espectro autista
Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders, impaired social interaction, language, and communication, which has increased worldwide in recent years. The deterioration of this condition occurs mainly at the brain level, currently it has been postulated that mitochondrial dysfunction, increased oxidative stress and decreased antioxidant defense leads to an imbalance in the ability to counteract the harmful effects of oxidative stress, such as oxidative degradation of lipids, proteins, and DNA that can cause damage to brain tissue, leading to the clinical symptoms and behaviors of ASD. Mitochondrial dysfunction can occur due to abnormalities in the electron transport chain, which induces and increases oxidative stress. On the other hand, the brain is extremely vulnerable to oxidative stress, due to its high oxygen consumption, its limited antioxidant capacity, and higher amounts of fatty acids and iron. This increased susceptibility of the brain to oxidative damage highlights the importance of understanding the role of oxidative stress in the clinical manifestations of ASD. Several studies have observed an increase in oxidative stress markers and a decrease in antioxidant enzymes in autism. Therefore, improving the oxidative state and maintaining the redox balance could improve the clinical manifestations of autism. The present study aims to carry out a narrative review on oxidative stress and mitochondrial dysfunction associated with ASD
Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders, impaired social interaction, language, and communication, which has increased worldwide in recent years. The deterioration of this condition occurs mainly at the brain level, currently it has been postulated that mitochondrial dysfunction, increased oxidative stress and decreased antioxidant defense leads to an imbalance in the ability to counteract the harmful effects of oxidative stress, such as oxidative degradation of lipids, proteins, and DNA that can cause damage to brain tissue, leading to the clinical symptoms and behaviors of ASD. Mitochondrial dysfunction can occur due to abnormalities in the electron transport chain, which induces and increases oxidative stress. On the other hand, the brain is extremely vulnerable to oxidative stress, due to its high oxygen consumption, its limited antioxidant capacity, and higher amounts of fatty acids and iron. This increased susceptibility of the brain to oxidative damage highlights the importance of understanding the role of oxidative stress in the clinical manifestations of ASD. Several studies have observed an increase in oxidative stress markers and a decrease in antioxidant enzymes in autism. Therefore, improving the oxidative state and maintaining the redox balance could improve the clinical manifestations of autism. The present study aims to carry out a narrative review on oxidative stress and mitochondrial dysfunction associated with ASD
Description
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Santiago, Chile
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Esta investigación no recibió ninguna
subvención específica de agencias de financiamiento de los
sectores público, comercial o sin fines de lucro
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Keywords
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Atribución-NoComercial-CompartirIgual 3.0 Chile (CC BY-NC-SA 3.0 CL)