Environmental pollutants such as heavy metals, endocrine-disrupting chemicals, microplastics, and airborne particulates are increasingly recognized for their potential to influence immune function through epigenetic mechanisms. This review examines conserved pollutant-associated pathways at interfaces of immunity and epigenetics, with particular attention to Toll-like receptor–NF-κB signalling, NLRP3 inflammasome activity, and reactive oxygen species-driven cascades. Evidence from cellular, animal, and epidemiological studies indicates that these pathways may converge on chromatin regulators such as DNA methyltransferases, histone deacetylases, and EZH2, leading to DNA methylation shifts, histone modifications, and altered chromatin accessibility. Pollutants are also reported to modulate non-coding RNAs, including miR-21, miR-155, and several lncRNAs, which can act as intermediaries between cytokine signalling and epigenetic remodelling. Findings from transgenerational models suggest that pollutant-linked immune–epigenetic alterations might persist across generations, raising the possibility of long-term consequences for immune and neurodevelopmental health. Comparative analyses further indicate convergence across diverse pollutant classes, pointing to a shared mechanistic axis of immune–epigenetic disruption. Overall, these insights suggest that pollutant-induced immune–epigenetic signatures may contribute to inflammation, altered immune responses, and heritable disease risks, and their clarification could inform biomarker discovery and future precision approaches in immunotoxicology.

Parkinson’s disease (PD) is a progressive neurological disorder marked by the gradual loss of dopamine-producing neurons in the brain. This neuronal degradation causes motor symptoms such as tremors, stiffness, and slowness of movement. Despite decades of research, current treatments remain limited to symptom management, highlighting the urgent need for deeper insights into PD mechanisms and new therapeutic approaches. Among model organisms, zebrafish (Danio rerio) have emerged as a valuable tool for PD research due to the possibility of genetic manipulation. Zebrafish can be engineered to carry human PD-associated mutations, such as those in α-synuclein, LRRK2, and Parkin, enabling researchers to study the molecular and cellular basis of the disease. Additionally, exposure to neurotoxins like MPTP and paraquat allows scientists to replicate PD-like symptoms in zebrafish, supporting drug screening and behavioural analysis. This review summarises the key advantages and limitations of zebrafish as a model for PD, compares it with rodent models, and discusses recent advances and future directions that may improve translational outcomes in PD therapy and personalised medicine.

Natamycin, a polyene macrolide antifungal, has long been used as a food preservative and is the only Food and Drug Administration (FDA)-approved topical treatment for fungal keratitis. While its safety is supported by specific ergosterol interaction and minimal systemic absorption, current research mainly focuses on short-term effects, often overlooking long-term, developmental, and microbiome-related impacts. In food applications, questions remain about cumulative exposure and potential disruptions to gut microbiota. For ophthalmology, advanced delivery methods like nanocarriers and hydrogels enhance drug penetration but may alter pharmacokinetics and pose formulation challenges. Regulatory approvals have historically depended on established safe use and limited toxicological data, emphasizing the need for more systematic evaluations. Zebrafish (Danio rerio) represent a promising yet underutilized model for addressing significant gaps in research, particularly in the realms of microbiome studies, ocular health, developmental processes, and multigenerational effects. When paired with omics technologies, zebrafish facilitate comprehensive system-level mapping of drug-induced outcomes. This review consolidates existing evidence and positions zebrafish as a vital translational link between in vitro assays, mammalian models, and clinical practice. Additionally, it proposes a framework to ensure the effective and scientifically supported use of natamycin in both food and medicinal applications.

Arthrospira platensis is a cyanobacterium of high nutraceutical value, notable for its rich protein, polyunsaturated fatty acids, essential minerals, vitamins, and bioactive pigments, including β-carotene, phycocyanin, and chlorophylls. This study evaluated the effect of agricultural hormones (AH)-indole-3-acetic acid (IAA), gibberellins (GA), and abscisic acid (ABA)-on β-carotenoid production. IAA was tested at 5 and 10 ppm. Under stable conditions, AH treatments enhanced growth, with IAA at 5 ppm achieving the highest density (1.2×106 filaments mL-1), significantly outperforming ABA and the controls (P < 0.05). Pigment responses varied: chlorophyll-a and b peaked at 10 ppm, while β-carotenoids were maximized at 5 ppm. Higher concentrations (>10 ppm) inhibited growth. Biomass from AH-treated cultures was incorporated into trout fry diets and tested over 50 days. Fish fed treated Arthrospira showed marked improvements, with body weight increasing from 2.70 ± 0.13 to 32.70 ± 4.11 g and length from 6.23 ± 0.09 to 13.84 ± 0.575 cm (P < 0.05). Diets containing IAA and ABA yielded the highest daily growth rates (463.4 and 406.39 mg d-1, respectively) compared to controls (323-334 mg d-1). Feed efficiency, food conversion rate, and condition factor were enhanced, with survival highest in the ABA group (98.3 vs. 85%). Under stress conditions, treated fish exhibited enhanced hematological and biochemical responses, including elevated white blood cell counts, glucose levels, and globulin levels. Superoxide dismutase activity in blood plasma was significantly higher (P < 0.05), ranging from 4.76 to 6.32 U mL-1. Overall, AH supplementation increased pigment yield in A. platensis and significantly enhanced growth, metabolism, antioxidant defense, and stress resilience in rainbow trout (Oncorhynchus mykiss) during early culture stages.

Potassium bromate (KBrO₃) is a known food additive and environmental pollutant with documented oxidative and genotoxic effects in mammals, yet its impact on aquatic organisms remains poorly characterized. To date, studies integrating behavioural, physiological, and histopathological endpoints for KBrO₃ toxicity in zebrafish have been limited. This study aimed to evaluate the acute and chronic toxicity of KBrO₃ in zebrafish (Danio rerio), focusing on behavioural and hepatic responses. Adult zebrafish were exposed to graded concentrations of KBrO₃ for 96 h following OECD Guideline 203 to determine median lethal concentration (LC₅₀) values. Behavioural parameters, including swimming speed, exploratory activity, and vertical zone preference, were analyzed. For chronic toxicity, fish were exposed to KBrO₃ for 21 days, and liver tissues were examined histologically following hematoxylin and eosin staining. Random blood glucose was measured immediately post-exposure. The 96-h LC₅₀ value for KBrO₃ was estimated as 1052.6 mg L⁻¹ . Acute exposure was associated with reduced locomotor activity, including decreases in swimming speed and exploration rate, along with increased bottom-zone activity. Chronic exposure (21 days) was associated with elevated blood glucose levels and hepatic alterations including vacuolization, sinusoidal dilation, hepatocellular degeneration, and necrosis. KBrO₃ exposure induced measurable behavioural, physiological, and hepatic alterations in zebrafish, demonstrating that sublethal biological effects occur at concentrations below those causing acute mortality. These findings provide baseline hazard characterization data for KBrO₃ in an aquatic vertebrate model and support future studies aimed at environmental risk assessment and mechanistic evaluation of bromate toxicity.