Mitochondrial dysfunction and oxidative stress in autism spectrum disorder: pharmacological insights into natural antioxidants

自闭症谱系障碍中的线粒体功能障碍和氧化应激:天然抗氧化剂的药理学见解

阅读:1

Abstract

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by social communication deficits, restricted and fixated interests and abnormal motor behaviors. Increasing evidence implicates oxidative stress, mitochondrial dysfunction, and neuroinflammation as key biological features of ASD. Aberrant redox homeostasis, reduced glutathione reserves, increased lipid peroxidation, and dysregulated NRF2 signaling have been documented in both peripheral tissues and brain samples. Post-mortem and imaging studies further reveal deficits in electron transport chain complexes and pyruvate dehydrogenase activity, suggesting a mechanistic link between mitochondrial bioenergetics and ASD-related phenotypes. These pathomechanisms have motivated interest in antioxidant metabolites from botanical drugs and nutrients as complementary strategies. To critically appraise mechanisms and levels of evidence (in vitro, in vivo, clinical) for vitamin E and C, glutathione and its precursors, polyphenols (quercetin, resveratrol, curcumin), Crocus sativus carotenoids (crocin/safranal), and "indirect" modulators (e.g., omega-3, folinic acid), emphasizing study quality, translational relevance, and limitations. The aim of this review is to synthesize current findings on the potential benefits of antioxidants in addressing both molecular and behavioral aspects of ASD, while also examining the link between oxidative stress and ASD. Furthermore, we discuss the role of antioxidant-based interventions in managing ASD symptoms. The review highlights the complex challenges associated with antioxidant therapies and deficiencies, emphasizing the need for a multifaceted nutritional approach particularly in children with ASD.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。