The Gut Microbiota And Oxidative Stress In Autism Spectrum ...

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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.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1

Figure 1

The connections among oxidative stress,…

Figure 1

The connections among oxidative stress, mitochondrial dysfunction, and dysfunction of GIT in autistic…

Figure 1 The connections among oxidative stress, mitochondrial dysfunction, and dysfunction of GIT in autistic children. The dysfunction of GIT in autistic children is related to mitochondrial dysfunction, and there is an interaction between oxidative stress and mitochondrial dysfunction. SCFAs, metabolites of the GIT microbiota, not only participate in the reaction process of oxidative stress but also can result in mitochondrial hyperactivity and further make mitochondria allergic to the oxidative stress.
Figure 2

Figure 2

Schematic representation of oxidative stress…

Figure 2

Schematic representation of oxidative stress in the brain.

Figure 2 Schematic representation of oxidative stress in the brain.
Figure 3

Figure 3

Relationships between the GIT microbiota…

Figure 3

Relationships between the GIT microbiota and ASD (the microbiota-gut-brain-axis). Note: BBB: blood-brain barrier;…

Figure 3 Relationships between the GIT microbiota and ASD (the microbiota-gut-brain-axis). Note: BBB: blood-brain barrier; ENS: enteric nervous system; GABA: γ-aminobutyric acid; HPA: hypothalamic-pituitary-adrenal; SCFAs: short-chain fatty acids.
Figure 4

Figure 4

Mitochondrial pathways involved in SCFAs…

Figure 4

Mitochondrial pathways involved in SCFAs as substrates. There are two different starting points…

Figure 4 Mitochondrial pathways involved in SCFAs as substrates. There are two different starting points in the electron cycle chain, i.e., Complex I and Complex II, which have their exclusive fuel sources. Notedly, Complexes III, IV, and IV are all involved in the abovementioned reactions; furthermore, butyrate and propionic acid enter into mitochondria to participate in related reaction via two crossed and overlapped pathways. Butyrate which resembles the glucose commonly enters into the citric acid (TCA) cycle via Acetyl-CoA, a key reaction substance. The TCA cycle mainly generates a kind of substrate of Complex I called Nicotinamide adenine dinucleotide (NADH). FADH2, as the substrate of Complex II, can be massively produced in two varied metabolic pathways which propionic acid participates in. Equally, propionic acid can produce some substrates of oxidative stress such as SCFAs et al. to be involved in related responses.
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References

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