Disfunción mitocondrial y estrés oxidativo asociado al trastorno del espectro autista: Una revisión narrativa

Abstract

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.