ISSUE FOCUS 42 FEED & ADDITIVE MAGAZINE May 2025 “The alterations caused by fumonisins in cellular metabolism have significant consequences in various tissues. For example, in the intestinal epithelium, inhibition of cell division and growth affects the turnover of epithelial cells, while induced apoptosis and weakening of tight junctions compromise the intestinal barrier, increasing permeability (leaky gut).” Despite advances in monitoring and mitigating mycotoxins, their presence in animal production remains a critical challenge due to their diversity and the impact of climate change, which predisposes higher concentrations of mycotoxins in feed and demands increasingly stringent and, above all, flexible control measures against these fungal-derived metabolites. Among mycotoxins, fumonisins, produced by Fusarium species, stand out due to their high global incidence, particularly in regions with warm and humid conditions that favor their development. Their impact on animal health and productivity is often underestimated in many production systems due to late detection and subclinical effects. Nevertheless, fumonisins affect key zootechnical parameters such as daily weight gain and conversion efficiency, and also cause immunosuppression that reduces resistance to diseases, leading to significant economic losses for producers. From a physiological perspective, fumonisins inhibit the enzyme ceramide synthase, which is essential for the proper metabolism of sphingolipids such as ceramide, sphingomyelin and glycosphingolipids. These molecules play critical roles in cellular biology, from membrane structure to signaling and regulation of vital functions. Inhibiting this enzyme leads to the excessive accumulation of sphinganine and sphingosine (Sa:So) in the cytoplasm, two molecules that, at high concentrations, are toxic to the body. This metabolic dysfunction disrupts signaling pathways at the cell membrane level, directly affecting cell differentiation and growth, as well as immune system function, since rapid cellular signaling is necessary to deal with infections or vaccines. Additionally, it predisposes to mitochondrial membrane dysfunction, resulting in overproduction of reactive oxygen species (ROS), inducing oxidative stress, damaging cellular structures, and activating pro-inflammatory pathways that ultimately compromise cellular function and trigger apoptosis. The alterations caused by fumonisins in cellular metabolism have significant consequences in various tissues. For example, in the intestinal epithelium, inhibition of cell division and growth affects TACKLING FUMONISINS: A NEW ERA IN ANIMAL HEALTH Mariano Gomory Junior Product Manager – Toxinbinder MIAVIT GmbH
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