H2 has shown anti-inflammatory and antioxidant ability in many clinical trials, and its application is recommended in the latest Chinese novel coronavirus pneumonia (NCP) treatment guidelines. Clinical experiments have revealed the surprising finding that H2 gas may protect the lungs and extrapulmonary organs from pathological stimuli in NCP patients. The potential mechanisms underlying the action of H2 gas are not clear. H2 gas may regulate the anti-inflammatory and antioxidant activity, mitochondrial energy metabolism, endoplasmic reticulum stress, the immune system, and cell death (apoptosis, autophagy, pyroptosis, ferroptosis, and circadian clock, among others) and has therapeutic potential for many systemic diseases. This paper reviews the basic research and the latest clinical applications of H2 gas in multiorgan system diseases to establish strategies for the clinical treatment for various diseases.

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.

Allergic diseases comprise a genetically heterogeneous cluster of immunologically mediated diseases, including asthma, food allergy (FA), allergic rhinitis (AR) and eczema, that have become major worldwide health problems. Over the past few decades, the spread of allergic diseases has displayed an increasing trend, and it has been reported that 22% of 1.39 billion people in 30 countries have a type of allergic disease. Undoubtedly, allergic diseases, which can be chronic, with significant morbidity, mortality and dynamic progression, impose major economic burdens on society and families; thus, exploring the cause of allergic diseases and reducing their prevalence is a top priority. Recently, it has been reported that the gastrointestinal (GI) microbiota can provide vital signals for the development, function, and regulation of the immune system, and the above-mentioned contributions make the GI microbiota a key player in allergic diseases. Notably, the GI microbiota is highly influenced by the mode of delivery, infant diet, environment, antibiotic use and so on. Specifically, changes in the environment can result in the dysbiosis of the GI microbiota. The proper function of the GI microbiota depends on a stable cellular composition which in the case of the human microbiota consists mainly of bacteria. Large shifts in the ratio between these phyla or the expansion of new bacterial groups lead to a disease-promoting imbalance, which is often referred to as dysbiosis. And the dysbiosis can lead to alterations of the composition of the microbiota and subsequent changes in metabolism. Further, the GI microbiota can affect the physiological characteristics of the human host and modulate the immune response of the host. The objectives of this review are to evaluate the development of the GI microbiota, the main drivers of the colonization of the GI tract, and the potential role of the GI microbiota in allergic diseases and provide a theoretical basis as well as molecular strategies for clinical practice.