Aflatoxins, toxic secondary metabolites produced primarily by Aspergillus flavus and Aspergillus parasiticus, pose a significant global health concern due to their frequent presence in crops, food, and feed—especially under climate change conditions. This review addresses the growing threat of aflatoxins by analyzing recent advances in detection and mitigation. A comprehensive literature review was conducted, focusing on bioremediation, physical and chemical detoxification, and fungal growth inhibition strategies. The occurrence of aflatoxins in water systems was also examined, along with current detection techniques, removal processes, and regulatory frameworks. Emerging technologies such as molecular diagnostics, immunoassays, biosensors, and chromatographic methods are discussed for their potential to improve monitoring and control. Key findings highlight the increasing efficacy of integrative approaches combining biological and technological solutions and the potential of AI-based tools and portable devices for on-site detection. Intelligent packaging and transgenic crops are also explored for their role in minimizing contamination at the source. Overall, this review emphasizes the importance of continued interdisciplinary research and the development of sustainable, adaptive strategies to mitigate aflatoxin risks, thereby supporting food safety and public health in the face of environmental challenges.

Aflatoxins, toxic secondary metabolites produced by Aspergillus species, are widespread contaminants in food and feed, with aflatoxin B1 (AFB1) recognized as the most potent carcinogen. Climate change increases the risk of contamination by promoting fungal proliferation. While the hepatotoxic and enterotoxic effects of aflatoxins are well established, emerging evidence highlights their immunosuppressive and neurotoxic potential. Notably, AFB1 disrupts gut microbiota, compromises intestinal barrier integrity, and induces neuroinflammation via the microbiota–gut–brain axis. Probiotics have shown promise in mitigating these effects by modulating microbial balance, enhancing barrier function, and reducing neuroinflammatory responses. This review summarizes current findings on the systemic toxicity of aflatoxins—particularly their impact on the gut–brain axis—and evaluates the therapeutic potential of probiotics in counteracting aflatoxin-induced damage.

Silymarin, a flavonolignan-rich extract of Silybum marianum, is widely recognized for its hepatoprotective potential. While rodent studies predominate, pigs (Sus scrofa) offer a more translationally relevant model due to their hepatic architecture, bile acid composition, and transporter expression, which closely resemble those of humans. This narrative review synthesises current evidence on the chemistry, pharmacokinetics, biodistribution, and hepatoprotective activity of silymarin in porcine models. Available studies demonstrate that when adequate intrahepatic exposure is achieved, particularly through optimised formulations, silymarin can attenuate oxidative stress, suppress inflammatory signalling, stabilise mitochondria, and modulate fibrogenic pathways. Protective effects have been reported across diverse porcine injury paradigms, including toxin-induced necrosis, ethanol- and diet-associated steatosis, metabolic dysfunction, ischemia–reperfusion injury, and partial hepatectomy. However, the evidence base remains limited, with few long-term studies addressing fibrosis or regeneration, and methodological heterogeneity complicates the comparison of data across studies. Current knowledge gaps in silymarin research include inconsistent chemotype characterization among plant sources, limited reporting of unbound pharmacokinetic parameters, and variability in histological scoring criteria across studies, which collectively hinder cross-study comparability and mechanistic interpretation. Advances in analytical chemistry, transporter biology, and formulation design are beginning to refine the interpretation of exposure–response relationships. Advances in analytical chemistry, transporter biology, and formulation design are beginning to refine the interpretation of exposure–response relationships. In parallel, emerging computational approaches, including machine-learning-assisted chemotype fingerprinting, automated histology scoring, and Bayesian exposure modeling, are being explored as supportive tools to enhance reproducibility and translational relevance; however, these frameworks remain exploratory and require empirical validation, particularly in modeling enterohepatic recirculation. Collectively, current porcine evidence supports silymarin as a context-dependent yet credible hepatoprotective agent, highlighting priorities for future research to better define its therapeutic potential in clinical nutrition and veterinary practice.

Genome instability can lead to a wide variety of diseases. Many endogenous and exogenous factors influence the level of damage to genetic material. Genome integrity depends on factors such as the fidelity of DNA replication, normal DNA organization in the chromosomes, and repair mechanisms. Genome stability influences fertility, embryonic development, and the maintenance of pregnancy. In the case of in vitro fertilization, it can be an important factor determining the success of the procedure. The aim of the study was to assess the stability of the genomes of recipient cows following in vitro fertilization using cytogenetic tests and to analyze the effects of selected vitamins and micro- and macroelements on genome integrity. Genome stability was analyzed using the sister chromatid exchange, fragile site, and comet assays. The material for analysis was peripheral blood from 20 Holstein-Friesian heifers that were embryo transfer recipients. The effect of selected micro- and macroelements and vitamins on the genome stability of the cows was analyzed. Folic acid was shown to significantly influence the level of damage identified using the SCE, FS, and SCGE assays, while iron affected SCE and SCGE results, and zinc affected FS.

Curcumin, the major polyphenolic constituent of Curcuma longa, has been widely investigated as a hepatoprotective adjunct due to its antioxidant and immunomodulatory properties. This review evaluates the relevance of curcumin for the prevention and management of liver dysfunction and hepatitis in pigs by synthesizing available porcine evidence and integrating mechanistic insights from translational liver injury models where pig-specific data remain limited. Across experimental hepatic injury contexts, curcumin administration is most consistently associated with reduced biochemical and structural indicators of hepatocellular damage, including decreased aminotransferase activity, attenuation of lipid peroxidation, and enhancement of endogenous antioxidant defenses. These effects are mechanistically linked to suppression of pro-inflammatory signaling pathways, particularly NF-κB-related transcriptional activity and inflammasome-associated responses, together with reduced expression of key cytokines such as TNF-α, IL-1β, and IL-6. Concurrent activation of Nrf2-centered cytoprotective pathways and induction of phase II antioxidant enzymes (including HO-1, GST, and NQO1) appear to constitute a conserved axis supporting hepatic oxidative stress resilience. In swine-relevant infectious settings, available data further support antiviral activity against selected porcine pathogens, including classical swine fever virus and porcine reproductive and respiratory syndrome virus, potentially mediated through interference with lipid-dependent stages of viral replication and modulation of Kupffer cell activation. Although combination strategies with established hepatoprotective approaches are conceptually attractive, current synergy evidence remains heterogeneous and largely extrapolated. Overall, curcumin represents a plausible adjunct candidate for supporting porcine liver health; however, translation into practice will depend on resolving formulation-dependent bioavailability constraints and strengthening the pig-specific evidence base.