Abstract
Autism spectrum disorders (ASDs) are a kind of neurodevelopmental disorder with rapidly increasing morbidity. In recent years, many studies have proposed a possible link between ASD and multiple environmental as well as genetic risk factors; nevertheless, recent studies have still failed to identify the specific pathogenesis. An analysis of the literature showed that oxidative stress and redox imbalance caused by high levels of reactive oxygen species (ROS) are thought to be integral parts of ASD pathophysiology. On the one hand, this review aims to elucidate the communications between oxidative stress, as a risk factor, and ASD. As such, there is also evidence to suggest that early assessment and treatment of antioxidant status are likely to result in improved long-term prognosis by disturbing oxidative stress in the brain to avoid additional irreversible brain damage. Accordingly, we will also discuss the possibility of novel therapies regarding oxidative stress as a target according to recent literature. On the other hand, this review suggests a definite relationship between ASD and an unbalanced gastrointestinal tract (GIT) microbiota (i.e., GIT dysbiosis). A variety of studies have concluded that the intestinal microbiota influences many aspects of human health, including metabolism, the immune and nervous systems, and the mucosal barrier. Additionally, the oxidative stress and GIT dysfunction in autistic children have both been reported to be related to mitochondrial dysfunction. What is the connection between them? Moreover, specific changes in the GIT microbiota are clearly observed in most autistic children, and the related mechanisms and the connection among ASD, the GIT microbiota, and oxidative stress are also discussed, providing a theory and molecular strategies for clinical practice as well as further studies.
Highlights
Autism spectrum disorders (ASDs), a loose umbrella term that includes a series of life-long heterogeneous clusters of neurodevelopmental disorders, is characterized by stereotyped behavior and deficits in social communication, interaction, and perception [1]
The gastrointestinal tract (GIT) dysfunction in autistic children is related to mitochondrial redox imbalance, i.e., mitochondrial dysfunction, and there is an interaction between oxidative stress and mitochondrial dysfunction [16, 17]
It is well documented that COX-2, as a vital enzyme that is overexpressed in tissues under oxidative stress, affects the metabolism of polyunsaturated acid (PUFA). ω-3 is considered to be connected with the high expression of COX-2
Summary
ASD, a loose umbrella term that includes a series of life-long heterogeneous clusters of neurodevelopmental disorders, is characterized by stereotyped behavior and deficits in social communication, interaction, and perception [1]. Last updated on July 11, 2016, the US Centers for Disease Control and Prevention (CDC https:// www.cdc.gov/) reported an incidence of 1 in 54 children worldwide; in addition, studies in Asia, Europe, and North America have identified individuals with ASD and shown an average prevalence of between 1% and 2% (see Table 1). It is conservatively estimated that the prevalence of ASD in China is 1%, among which more than 2 million children aged 0-14 years have the disease [2]. There is no practical and targeted treatment for ASD, which has become a major worldwide health problem [4]. Much evidence indicates that oxidative stress plays a vital role in the pathophysiology of nervous and mental diseases, in ASD [6,7,8,9]. Anecdotal reports have suggested that oxidative stress response is crucially important
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