Disruption of sphingolipid metabolism and induction of equine leukoencephalomalacia by Fusarium proliferatum culture material containing fumonisin B(2) or B(3).
Abstract: Fumonisin B(1), B(2), and B(3) are inhibitors of ceramide synthase, a key enzyme in the pathway for de novo sphingolipid biosynthesis. Corn, naturally contaminated with either predominantly fumonisin B(1) or pure fumonisin B(1), has been shown to cause equine leukoencephalomalacia (ELEM). It has been hypothesized that fumonisin-induced disruption of sphingolipid metabolism is an early event in the development of ELEM. Recently, it was shown that Fusarium proliferatum corn culture diets containing predominantly fumonisin B(2), but not diets which were predominantly fumonisin B(3), at 75 ppm (0.75 mg/kg BW/day) caused hepatotoxicity and ELEM. Analysis of free sphingoid bases and complex sphingolipids in serum, liver, and kidney, revealed that both the fumonisin B(2) and B(3) diets caused significant disruption of sphingolipid metabolism, however, the fumonisin B(2) culture material diet was significantly more effective than the fumonisin B(3) culture material diet at disrupting sphingolipid metabolism and in causing hepatotoxicity and clinical signs indicative of the onset of ELEM. A significant increase in the ratio of free sphinganine to free sphingosine in serum was first evident at day 4 and 11 with the fumonisin B(2) and B(3) diets, respectively. Increase in serum enzymes indicative of liver toxicity was first evident at day 34 in ponies fed the fumonisin B(2) diet and clinical signs (head shaking, gait problems, and muscle tremors) were first observed at day 48. Ponies fed the fumonisin B(3) diets showed no increase in serum enzymes or clinical signs for as long as 65 days when the study with fumonisin B(3) was stopped. The results support the conclusion fumonisin B(2) is more effective than fumonisin B(3) in disrupting sphingolipid metabolism and induction of ELEM and liver injury in ponies.
Publication Date: 1997-07-01 PubMed ID: 21781781DOI: 10.1016/s1382-6689(97)00015-xGoogle Scholar: Lookup
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Summary
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The research article explores the harmful effects of Fusarium proliferatum dietary culture which contain fumonisin B2 or B3 on horses. It suggests that fumonisin B2 is more effective than B3 in creating a disruption in sphingolipid metabolism, causing liver damage and equine leukoencephalomalacia, a serious neurological condition in horses.
Fumonisin B(2) and B(3) and Their Roles in Sphingolipid Metabolism
Fumonisin B(1), B(2), and B(3) are known inhibitors of ceramide synthase, an enzyme crucial for de novo sphingolipid synthesis. The research delves into how these compounds, particularly B(2) and B(3), when found in corn cultures affected by Fusarium proliferatum, can affect sphingolipid metabolism and therefore horse health.
- Fumonisin-induced disruption of sphingolipid metabolism is considered to be an early event in the inception of equine leukoencephalomalacia (ELEM).
- The study found both fumonisin B(2) and B(3) diets caused significant disruption of sphingolipid metabolism, but fumonisin B(2) was notably more effective.
Fumonisin B(2) and B(3) and Their Effects on Horse Health
The in-depth analysis of this study indicated a profound impact of fumonisin B(2) and B(3) on horse health, manifesting in liver toxicity and symptoms indicative of ELEM.
- It was found that the fumonisin B(2) diet resulted in hepatotoxicity and early signs of ELEM.
- Clinical symptoms of ELEM like head shaking, gait problems, and muscle tremors surfaced at day 48 in horses fed on the fumonisin B(2) diet.
- Meanwhile, horses on the fumonisin B(3) diet showed no immediate increase in serum enzymes or clinical signs relating to liver damage or ELEM for as long as 65 days.
- Thus, fumonisin B(2) was proven to be more effective than fumonisin B(3) in causing disruptions in sphingolipid metabolism, liver injuries, and in inducing ELEM in horses.
Conclusion
This research substantiates the harmful effects of specific fumonisins in disrupting crucial metabolic pathways in horses, leading to severe illnesses. The findings are crucial for understanding the onset of such diseases, potentially aiding in devising methods to circumvent these problems.
Cite This Article
APA
Riley RT, Showker JL, Owens DL, Ross PF.
(1997).
Disruption of sphingolipid metabolism and induction of equine leukoencephalomalacia by Fusarium proliferatum culture material containing fumonisin B(2) or B(3).
Environ Toxicol Pharmacol, 3(3), 221-228.
https://doi.org/10.1016/s1382-6689(97)00015-x Publication
Researcher Affiliations
- United States Department of Agriculture, Agricultural Research Service, Toxicology and Mycotoxin Research Unit, P.O. Box 5677, Athens, GA 30604-5677, USA.
Citations
This article has been cited 6 times.- Marzougui Z, Huet S, Blier AL, Hégarat LL, Tounsi-Kettiti H, Kharrat R, Marrouchi R, Fessard V. Investigation of the Genotoxic Potential of the Marine Toxin C17-SAMT Using the In Vivo Comet and Micronucleus Assays. Mar Drugs 2022 Sep 30;20(10).
- Mohan J, Sheik Abdul N, Nagiah S, Ghazi T, Chuturgoon AA. Fumonisin B(2) Induces Mitochondrial Stress and Mitophagy in Human Embryonic Kidney (Hek293) Cells-A Preliminary Study. Toxins (Basel) 2022 Feb 25;14(3).
- Knutsen HK, Barregård L, Bignami M, Brüschweiler B, Ceccatelli S, Cottrill B, Dinovi M, Edler L, Grasl-Kraupp B, Hogstrand C, Hoogenboom LR, Nebbia CS, Petersen A, Rose M, Roudot AC, Schwerdtle T, Vleminckx C, Vollmer G, Wallace H, Dall'Asta C, Gutleb AC, Humpf HU, Galli C, Metzler M, Oswald IP, Parent-Massin D, Binaglia M, Steinkellner H, Alexander J. Appropriateness to set a group health-based guidance value for fumonisins and their modified forms. EFSA J 2018 Feb;16(2):e05172.
- Voss KA, Plattner RD, Riley RT, Meredith FI, Norred WP. In vivo effects of fumonisin B1-producing and fumonisin B1-nonproducing Fusarium moniliforme isolates are similar: fumonisins B2 and B3 cause hepato- and nephrotoxicity in rats. Mycopathologia 1998;141(1):45-58.
- Tomaszewska E, Dobrowolski P, Dajnowska A, Arbatowska L, Puzio I, Rudyk H, Brezvyn O, Kotsyumbas I, Donaldson J, Śliwa J, Arciszewski MB, Muszyński S. The effect of prenatal fumonisin B exposure on bone innervation in newborn Wistar rats. J Vet Res 2024 Dec;68(4):633-642.
- Ando M, Yamaguchi H, Iwashita N, Takagi Y, Yoshinari T, Fukuyama T. Oral Exposure to Low Concentration of Fumonisin B2, but Not Fumonisin B1, Significantly Exacerbates the Pathophysiology of Imiquimod-Induced Psoriasis in Mice. Int J Mol Sci 2024 Jul 18;25(14).
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