Within the pediatric population, bronchial asthma is one of the most prevalent chronic respiratory system diseases. The number of exacerbations, severity, and duration of symptoms all have a significant impact on children’s life quality. In the last decades, the prevention and management strategies of this pathology have focused on maintaining or even increasing the pulmonary function to maximum levels in early childhood, as it has been demonstrated that functional deficits at this level occurring before school age cause pathological manifestations later, in adulthood. The epithelium of the airways and implicitly that of the lung is the first barrier against the lesions caused by pro-oxidative factors. Both oxidative and antioxidative factors can be of endogenous origin (produced by the body) or exogenous (from the environment or diet). Good functioning of antioxidant defense mechanisms from the molecular level to the tissue level, and a balance between pro-oxidative factors and anti- oxidative factors, influence the occurrence of compensatory mechanisms at the level of the respiratory epithelium, causing the delay of local responses to the stress induced by chronic inflammation (bronchial remodeling, thickening of airway smooth muscles, bronchoconstriction, bronchial hyper-reactivity). These mechanisms underlie the pathophysiological changes in asthma. Numerous studies carried out among the pediatric population inclusively have demonstrated the effectiveness of antioxidants in the prophylaxis, slowing down and preventing the progression of this pathology. This review complements the scientific articles, aiming at emphasizing the complexity of oxidative physio-pathological pathways and their importance in the occurrence, development, and therapeutic response in asthma, providing a good understanding of the relationship between oxidative and antioxidative factors, and being a source of future therapeutic strategies.

Background: Childhood obesity has become a major public health concern worldwide. Increasing evidence suggests that alterations in the gut microbiome may play a significant role in the development and progression of pediatric obesity. This narrative review synthesizes and analyzes recent studies investigating microbiome alterations in children with obesity, highlighting emerging insights and their potential implications for disease management. Understanding the relationship between gut microbial composition and obesity may provide new perspectives for prevention and therapeutic strategies in overweight pediatric populations. This narrative review was conducted through a search of major biomedical databases, including PubMed and Web of Science, complemented by manual screening of reference lists of relevant articles. Key findings: Children affected by obesity exhibit significant changes in gut microbiome composition, characterized by reduced microbial diversity and predominance of the Firmicutes and Bacteroidetes phyla. The balance between these two bacterial groups appears critical for maintaining gut homeostasis. Studies consistently report an increased Firmicutes-to-Bacteroidetes ratio in children with elevated body weight, suggesting that disruption of this balance may contribute to metabolic dysregulation and obesity-related pathologies. Given the essential role of the gut microbiota in nutrient metabolism and energy extraction, dysbiosis in obesity is associated with enhanced energy harvest and lipid absorption. Certain bacterial populations may promote increased caloric uptake, thereby contributing to weight gain and adiposity. Multidimensional interventions, including dietary modification and physical activity, have demonstrated the potential to reduce obesogenic microbiota patterns and restore microbial diversity. Additionally, probiotic supplementation is being investigated as a strategy to reestablish microbial homeostasis and potentially support body mass index reduction. Despite promising findings, further research is required to clarify mechanisms, establish causality, and determine the clinical effectiveness of microbiome-targeted therapies before they can be fully integrated into the management of pediatric obesity.

Childhood obesity is linked to heightened oxidative stress, a key driver of endothelial dysfunction, inflammation, and metabolic complications. Antioxidants, including Vitamins C and E, are vital in neutralizing free radicals and mitigating oxidative damage. This non-systematic review examines the potential advantages of antioxidant supplementation in pediatric obesity, focusing on its effects on vascular health, insulin sensitivity, and inflammatory processes. Emerging data suggest that antioxidants may improve endothelial function, reduce blood pressure, and enhance metabolic homeostasis in obese children. However, the long-term efficacy and safety of antioxidant supplementation remain uncertain, necessitating further rigorous randomized controlled trials. A deeper understanding of antioxidants’ role in pediatric obesity could unlock novel therapeutic approaches for managing obesity-related complications and improving children’s overall health outcomes.

Recent research has generated awareness of the existence of various pathophysiological pathways that contribute to the development of chronic diseases; thus, pro-oxidative factors have been accepted as significant contributors to the emergence of a wide range of diseases, from inflammatory to malignant. Redox homeostasis is especially crucial in liver pathology, as disturbances at this level have been linked to a variety of chronic diseases. Hepatitis is an umbrella term used to describe liver inflammation, which is the foundation of this disease regardless of its cause. Chronic hepatitis produces both oxidative stress generated by hepatocyte inflammation and viral inoculation. The majority of hepatitis in children is caused by a virus, and current studies reveal that 60–80% of cases become chronic, with many young patients still at risk of advancing liver damage. This review intends to emphasize the relevance of understanding these pathological redox pathways, as well as the need to update therapeutic strategies in chronic liver pathology, considering the beneficial effects of antioxidants.

Type 1 Diabetes (T1D) is a complex autoimmune disorder characterized by immune-mediated destruction of pancreatic β cells, driven by genetic susceptibility and modulated by environmental factors, notably the gut microbiome. Dysbiosis, manifested as reduced microbial diversity, perturbations in the Firmicutes/Bacteroidetes ratio, and compromised short-chain fatty acid production, contributes to T1D pathogenesis through mechanisms involving immune system dysregulation and heightened intestinal permeability. Emerging evidence indicates a relationship between the gut and oral microbiomes, as well as the potential influence of the virome and mycobiome. This narrative review synthesizes the current literature on the intricate interplay between the gut microbial ecosystem, the host immune response, and the development of T1D, highlighting the potential for targeted microbiome-based interventions to ameliorate disease progression. A more nuanced understanding of these multi-kingdom interactions is essential for developing precise therapeutic strategies to prevent or delay T1D onset and to improve patient outcomes through restoration of immune tolerance and gut homeostasis.

Pediatric obstructive sleep apnea syndrome (OSAS) is a common sleep-related breathing disorder increasingly recognized as a multisystem disease rather than an isolated disorder of the upper airway. Recurrent episodes of upper airway obstruction generate intermittent hypoxia, reoxygenation, and sleep fragmentation, promoting excessive production of reactive oxygen and nitrogen species and disruption of antioxidant defenses. This narrative review summarizes current evidence regarding the mechanisms, biomarkers, and clinical consequences of oxidative stress in pediatric OSAS. Intermittent hypoxia activates several redox-sensitive pathways, including NADPH oxidases, hypoxia-inducible factor-1α, nuclear factor-κB, mitochondrial dysfunction, and endoplasmic reticulum stress, thereby creating a bidirectional relationship between oxidative stress and systemic inflammation. Pediatric studies have demonstrated alterations in lipid peroxidation products, glutathione redox balance, urinary 8-hydroxy-2′-deoxyguanosine, isoprostanes, NOX2-related markers, and inflammatory mediators. These abnormalities are associated with endothelial dysfunction and cardiovascular, neurocognitive, metabolic, hepatic, renal, and immune consequences, and several may improve following effective treatment. Importantly, the magnitude of oxidative and end-organ injury does not consistently parallel the apnea-hypopnea index, suggesting that hypoxic burden, obesity, genetic susceptibility, antioxidant capacity, and disease duration influence individual biological vulnerability. Although several oxidative biomarkers show potential for disease characterization and treatment monitoring, methodological heterogeneity and the absence of standardized pediatric reference values currently limit their clinical application. Future integration of polysomnographic hypoxic-burden metrics with oxidative, inflammatory, metabolomic, and genomic biomarkers may improve risk stratification and facilitate more personalized management of pediatric OSAS.