Cervical cancer ranks third among malignant diseases of the female reproductive system and progressively develops through a series of pathological changes known as cervical intraepithelial neoplasia (CIN). Despite being extremely aggressive and causing increased mortality, the main treatment options include surgery or a combination of chemotherapy and radiotherapy, often based on cisplatin-based chemotherapy and external beam radiotherapy or brachytherapy. Cervical dysplasia is an abnormal growth of cells on the surface of the cervix that could lead to cervical cancer. CIN most commonly occurs at the squamocolumnar junction of the cervix, a transitional zone between the squamous epithelium of the vagina and the columnar epithelium of the endocervix. The primary cause of CIN is chronic infection of the cervix with Human Papillomavirus (HPV). Oxidative stress (OS) and chronic inflammation are associated with HPV-induced cervical dysplasia. Reactive oxygen species (ROS) facilitate the progression of CIN through DNA damage, immune evasion, and cellular mutations. Thus, the inflammatory environment, characterized by increased expression of proinflammatory cytokines, contributes to epithelial transformation. Given these mechanisms, antioxidants, including vitamins A, C, D, E, polyphenols, and carotenoids, are being investigated for their potential as adjunctive therapies in CIN management. This review aims to provide a comprehensive analysis of the influence of oxidative stress, antioxidants, and inflammation on cervical cancer.

Background/Objectives: Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset neurodevelopmental disorder, characterized by difficulty maintaining attention, impulsivity, and hyperactivity. While the cause of this disorder is still unclear, recent studies have stated that heredity is important in the development of ADHD. This is linked to a few comorbidities, including depression, criminal behavior, and anxiety. Although genetic factors influence ADHD symptoms, there are also non-genetic factors, one of which is oxidative stress (OS), which plays a role in the pathogenesis and symptoms of ADHD. This review aims to explore the role of OS in ADHD and its connection to antioxidant enzyme levels, as well as the gut–brain axis (GBA), focusing on diet and its influence on ADHD symptoms, particularly in adults with comorbid conditions. Methods: The literature search included the main available databases (e.g., Science Direct, PubMed, and Google Scholar). Articles in the English language were taken into consideration and our screening was conducted based on several words such as “ADHD”, “oxidative stress”, “diet”, “gut–brain axis”, and “gut microbiota.” The review focused on studies examining the link between oxidative stress and ADHD, the role of the gut–brain axis, and the potential impact of dietary interventions. Results: Oxidative stress plays a critical role in the development and manifestation of ADHD symptoms. Studies have shown that individuals with ADHD exhibit reduced levels of key antioxidant enzymes, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), as well as a diminished total antioxidant status (TOS) compared to healthy controls. Additionally, there is evidence of a close bidirectional interaction between the nervous system and gut microbiota, mediated by the gut–brain axis. This relationship suggests that dietary interventions targeting gut health may influence ADHD symptoms and related comorbidities. Conclusions: Oxidative stress and the gut–brain axis are key factors in the pathogenesis of ADHD, particularly in adults with comorbid conditions. A better understanding of these mechanisms could lead to more targeted treatments, including dietary interventions, to mitigate ADHD symptoms. Further research is required to explore the therapeutic potential of modulating oxidative stress and gut microbiota in the management of ADHD.

Tartrazine (TZ, also known as FD&C Yellow No. 5 or E102) is a synthetic, water-soluble yellow food dye widely used in the food and pharmaceutical industries. Some studies have associated TZ with allergic reactions, especially among people with dye sensitivities or pre-existing allergies. Recent research also suggests a possible link between TZ consumption and the worsening of behavioral disorders, especially in children, including symptoms such as hyperactivity, irritability, restlessness, and sleep disturbances. Experimental studies in laboratory animals have highlighted potential risks associated with prolonged or high-dose exposure, including toxic effects on the nervous system and liver function. In addition, increasing evidence indicates that TZ can induce oxidative stress (OS) by increasing the production of reactive oxygen species (ROS), which can contribute to cellular damage and inflammation. Although the evidence remains inconclusive, there are recommendations to limit the intake of synthetic food dyes, especially in children’s diets. The purpose of this review is to examine the potential toxic effects on health of tartrazine by analyzing findings from experimental studies in cell cultures and laboratory animals, as well as correlations observed in humans. We focus on documented adverse reactions, including possible neurotoxic, hepatotoxic, oxidative, and behavioral effects. Through this, we aim to contribute to a more comprehensive understanding of the risks associated with exposure to this synthetic food dye.

Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset neurodevelopmental disorder characterized by difficulty maintaining attention, impulsivity and hyperactivity. Although the cause of this disorder is still unclear, recent studies state that heredity is important in the development of ADHD. This is linked to a few comorbidities: depression, criminal behavior and anxiety. Although genetic factors play a major role in the pathogenesis of ADHD, there are also non-genetic factors, one of which would be oxidative stress (OS) that are associated with ADHD. OS is implicated in the pathogenesis of ADHD, through lower levels of antioxidant enzymes such as glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), as well as a lower total antioxidant status (TOS) compared to control groups. Moreover, there is a close bidirectional connection between the nervous system and the intestinal microbiota, and the communication between the two systems is carried out through the gut-brain axis (GBA). A thorough review of diet, OS implications, mechanism of action, pharmacokinetics, and drug-drug interactions are reviewed here, with a special focus on treatment in adults with comorbid conditions.

Tartrazine (TZ, also known as FD&C Yellow No. 5 or E102) is a synthetic, water-soluble yellow food dye widely used in the food and pharmaceutical industries. Some studies have associated TZ with allergic reactions, especially among people with dye sensitivities or pre-existing allergies. Recent research also suggests a possible link between TZ consumption and the worsening of behavioral disorders, especially in children, including symptoms such as hyperactivity, irritability, restlessness, and sleep disturbances. Experimental studies in laboratory animals have highlighted potential risks associated with prolonged or high-dose exposure, including toxic effects on the nervous system and liver function. In addition, increasing evidence indicates that TZ can induce oxidative stress (OS) by increasing the production of reactive oxygen species (ROS), which can contribute to cellular damage and inflammation. Although the evidence remains inconclusive, there are recommendations to limit the intake of syn-thetic food dyes especially in children’s diets. The purpose of this review is to examine the potential toxic effects on health of tartrazine by analyzing findings from experimental studies in cell cultures and laboratory animals, as well as correlations observed in humans. We focus on documented adverse reactions, including possible neurotoxic, hepatotoxic, oxidative, and behavioral effects. Through this, we aim to contribute to a more comprehensive understanding of the risks associated with exposure to this syn-thetic food dye.

Caffeine is one of the most widely consumed psychoactive stimulants, primarily functioning as a non-selective adenosine receptor antagonist. Its increasing detection in wastewater and surface waters reflects extensive anthropogenic use. This review synthesizes evidence from zebrafish (Danio rerio)—a genetically tractable vertebrate with rapidly developing external embryos—to assess the impact of caffeine exposure across environmentally relevant (ng–µg/L) and pharmacological/toxicological (mg/L and above) concentrations on early development and neurobehavior. Behavioral studies indicate dose- and stage-dependent alterations in locomotion, anxiety-like responses, memory performance, and sleep patterns, suggesting disruptions in neural circuitry and stress-axis regulation. Biochemical analyses frequently reveal oxidative imbalances characterized by increased reactive oxygen species and lipid peroxidation, alongside changes in antioxidant defenses (e.g., glutathione levels, superoxide dismutase (SOD) activity, and glutathione reductase activity). These findings support oxidative stress as a potential mechanistic hub, although a causal relationship has yet to be established. Embryonic exposure to caffeine is associated with developmental toxicity, including delayed hatching and concentration-dependent malformations such as edema, axial deformities, impaired angiogenesis, and neuromuscular defects at higher doses. However, cross-study comparisons are hindered by variations in units, exposure durations, and assay protocols. In summary, caffeine disrupts behavior, redox homeostasis, and developmental processes in zebrafish, highlighting the necessity for standardized methodologies to identify stage-specific vulnerabilities.