Toxic Mechanism and Biological Detoxification of Fumonisins

Abstract

Food safety is related to the national economy and people’s livelihood. Fumonisins are widely found in animal feed, feed raw materials, and human food. This can not only cause economic losses in animal husbandry but can also have carcinogenicity or teratogenicity and can be left in animal meat, eggs, and milk which may enter the human body and pose a serious threat to human health. Although there are many strategies to prevent fumonisins from entering the food chain, the traditional physical and chemical methods of mycotoxin removal have some disadvantages, such as an unstable effect, large nutrient loss, impact on the palatability of feed, and difficulty in mass production. As a safe, efficient, and environmentally friendly detoxification technology, biological detoxification attracts more and more attention from researchers and is gradually becoming an accepted technique. This work summarizes the toxic mechanism of fumonisins and highlights the advances of fumonisins in the detoxification of biological antioxidants, antagonistic microorganisms, and degradation mechanisms. Finally, the future challenges and focus of the biological control and degradation of fumonisins are discussed.

Efficacy of Bentonite and Fumonisin Esterase in Mitigating the Effects of Aflatoxins and Fumonisins in Two Kenyan Cattle Breeds

“…Aflatoxin M1 (AFM1) is the monohydroxylated metabolite of AFB1 which is similarly toxic and carcinogenic and is secreted in the milk of cows fed on AFB1-contaminated diets. , Analysis of AFM1 in milk is therefore of importance in checking for food safety and AFB1 exposure, using several methods including chromatography. This carry-over of AFB1 to milk as AFM1 ranges from less than 1% to 6.2% and may be affected by, among other factors, the level of milk production, breed, and presence of other mycotoxins. − Fumonisins on the other hand are not excreted in milk but have a synergistic effect when they co-occur with AF in pigs , and humans in the induction of liver disease . Hence, we hypothesize that the co-occurrence of AF and FUM may increase the uptake of AF and its subsequent carry-over to milk.…”

“…This carry-over of AFB1 to milk as AFM1 ranges from less than 1% to 6.2% and may be affected by, among other factors, the level of milk production, breed, and presence of other mycotoxins. 24−27 Fumonisins on the other hand are not excreted in milk but have a synergistic effect when they co-occur with AF in pigs 13,28 and humans in the induction of liver disease. 29 Hence, we hypothesize that the co-occurrence of AF and FUM may increase the uptake of AF and its subsequent carry-over to milk.…”

“…Once absorbed, AF or their metabolites can be detected in plasma and are useful biomarkers of exposure. , Ruminants are more tolerant to FUM, but at the exposure of high doses over a longer time, effects such as reduced feed intake, decrease in milk yield, hepatotoxicity, nephrotoxicity, and reproduction effects have been reported. − Structurally, FUM are similar to sphingosine (So) and sphinganine (Sa) and interfere with sphingoid bases metabolism by blocking ceramide synthase causing an increase in intercellular free Sa . Therefore, this variation of Sa/So ratio characterized by elevated Sa in blood and urine samples may be used as a biomarker of exposure and effect of FUM. − The liver is the main target organ for both AF and FUM, resulting in impairment of protein synthesis leading to reduced levels of plasma proteins and amino acids, and causing anemia, lymphocytopenia, and monocytopenia. − AF further affects the liver with plasma glutamic oxalacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), γ-glutamyl transferase (GGT), and alkaline phosphatase (ALP) used as biochemical indicators. ,, Long-term low-level exposure to FUM elevates serum aspartate aminotransferase (AST) and GGT . However, little has been done to show the impact of FUM on hematological and biochemical parameters in dairy cattle.…”

Fumonisin B1-Induced Oxidative Burst Perturbed Photosynthetic Activity and Affected Antioxidant Enzymatic Response in Tomato Plants in Ethylene-Dependent Manner

“…However, our findings reported that the ET emission is dependent on the applied FB1 concentration in both mature tomato genotypes after 72 h which could contribute to higher lipid peroxidation and EL from WT leaves. High lipid peroxidation (expressed in terms of MDA) directly corresponds to enhanced oxidative stress producing more reactive lipid peroxide radicals and disrupting structural and functional properties of lipids under FB1 stress (Qu et al 2022). Likewise, more EL from FB1-treated leaves denotes cell death induced by an oxidative burst and is dependent on the applied concentration of FB1 (Otaiza-González et al 2022).…”

Recent Research on Fusarium Mycotoxins in Maize—A Review

“…The main aspect of fumonisin toxicity is the inhibition of ceramide synthesis and the disruption of sphingolipid metabolism, which can cause cell apoptosis [ 122 ]. This mechanism of action stems from the similarity between the chemical structure of fumonisins and the structure of sphingosine (the primary part of sphingolipids), which is why they are recognised, and bound, by ceramide synthase [ 123 ].…”