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ARS Home » Southeast Area » Athens, Georgia » U.S. National Poultry Research Center » Toxicology & Mycotoxin Research » Research » Publications at this Location » Publication #309486
Title: Fumonisins, Tortillas and Neural Tube Defects: Untangling a Complex Issue

Author
item Voss, Kenneth
item Riley, Ronald
item GELINEAU-VAN WAES, JANEE - Creighton University

Submitted to: Corn Utilization Conference Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 6/2/2014
Publication Date: 6/2/2014
Citation: Voss, K.A., Riley, R.T., Gelineau-Van Waes, J.B. 2014. Fumonisins, Tortillas and Neural Tube Defects: Untangling a Complex Issue. Corn Utilization and Technology Conference. June 2-4, 2014. Lousiville, Kentucky.

Interpretive Summary:

Technical Abstract: Fumonisin mycotoxins are found in corn and corn-based foods. Fumonisin B1 (FB1), the most common, disrupts sphingolipid metabolism thereby causing species-specific diseases in animals that include cancer in rodents and (birth) neural tube defects (NTD) in LM/Bc mice. Fumonisins’ affect on human health is uncertain. Nonetheless, evidence suggests they contribute to the risk of NTD in populations consuming large amounts of tortillas made from fumonisin-contaminated corn. A series of bioassays have therefore been done to investigate how the alkaline cooking method for making tortillas, known as nixtamalization, influences FB1 bioavailability and toxicity. 1. Portions of three batches of corn having low-, mid- or high-levels of FB1 were nixtamalized: alkaline cooking reduced FB1 concentrations in all three batches by >90%. When fed to rats, no evidence of toxicity was found in groups fed the nixtamalized low- or mid-level corn. FB1-related kidney lesions and sphingolipid effects were found in rats fed the high-level nixtamalized corn but they were significantly less severe than those found in all groups fed the batches of uncooked, contaminated corn. 2. The alkaline conditions of nixtamalization convert FB1 to hydrolyzed FB1 (HFB1) and variable amounts of HFB1 are found in tortillas. The NTD-induction potential of HFB1 was compared to that of FB1 using the LM/Bc mouse bioassay. A maternal dose of 10 mg/kg body weight FB1 induced a high incidence of NTD, significantly reduced fetal weights, caused maternal liver lesions, and markedly disrupted sphingolipid metabolism. Up to 20 mg/kg body weight HFB1 in contrast did not induce NTD, fetal toxicity or maternal liver lesions and only the high dose had a minimal effect on sphingolipid metabolism. 3. There is evidence that NTD induction in LM/Bc mice by FB1 involves disruption of folate (folic acid supplementation reduces the risk of NTD)-dependent processes and that folic acid levels are reduced when making tortillas. Feeding trials were conducted to determine if consumption of a folate deficient diet for five weeks prior to mating modulates (10 mg/kg maternal body weight) FB1-dependent NTD induction in LM/Bc mice. Consumption of the folate deficient diet depleted maternal blood and plasma folate concentrations by 80% or more (measured at necropsy on gestation day 16). However, the deficient diet did not exacerbate NTD induction by FB1 but rather reduced the number of affected litters and fetuses, suggesting that it may have offered some degree of protection. Together, these findings show that nixtamalization reduces fumonisin toxicity and contribute to determining the mechanistic, nutritional, and other factors that modulate FB1-dependent NTD induction in the LM/Bc mouse model.