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Nixtamalization Reduces Fumonisin Toxicity

July 2014

Fumonisins are found in corn and in foods prepared from corn. Fumonisin B1, the most common of these Fusarium mycotoxins, causes diseases in farm and laboratory animals, and is a suspected risk factor for neural tube defects (serious, often fatal birth defects) in humans that depend on corn that may be contaminated as a diet staple. Among the research findings showing evidence for the latter are the results of a study conducted in the aftermath of a cluster of neural tube defects that occurred in southeastern Texas during 1990-1991. The findings included associations between moderate consumption of tortillas (defined as at least 301 but not more than 400) during the first trimester of pregnancy, biomarker-based indications of fumonisin exposure, and an increased risk of neural tube defects.

Tortillas, snacks, and other foods containing corn are made by the traditional cooking process known as nixtamalization. The process involves cooking the corn kernels in alkaline water (alkalinity provided by cooking lime), rinsing with water, and grinding. The resulting masa is dried to make masa flour or cooked to make tortillas or other foods. Nixtamalization reduces fumonisin concentrations in masa and its products by 50% or more compared to the uncooked corn through a combination of extraction into the cooking liquid and the chemical process of hydrolysis.

Because hydrolyzed fumonisins and perhaps other unknown fumonisin reaction products remain in masa after nixtamalization, a cooperative research initiative was undertaken by the USDA-ARS Toxicology and Mycotoxin Research Unit and the Department of Pharmacology, Creighton University to test whether or not nixtamalization reduces toxicity using in vivo bioassays based on fumonisin-specific endpoints in well-characterized animal models.

Fumonisin B1 causes neural tube defects in the LM/Bc mouse strain when given at a critical time during pregnancy. The first study, therefore, compared the ability of fumonisin B1 and its hydrolyzed form (HFB1) to induce neural tube defects in this animal model. Neural tube defects were found in all ten litters and in two-thirds of the fetuses from females that were treated with 10 mg/kg body weight fumonisin B1. In contrast, maternal doses of up to 20 mg/kg body weight HFB1 did not cause neural tube defects. Furthermore, indications of significant maternal toxicity, including cell death in liver and changes in tissue sphingolipid levels, were found in females given fumonisin B1, but were absent (liver cell death) to minimal (sphingolipid effects) in females given HFB1.

In the second study, three batches of corn containing increasing levels (designated low, mid or high) of fumonisin B1 were used to assess how nixtamalization affects kidney toxicity in male rats. The animals were fed diets containing uncooked or nixtamalized corn (50/50 by weight, mixed with rodent chow) for three weeks. Microscopic kidney lesions and significantly elevated sphingoid base concentrations (a biomarker of exposure) characteristic of fumonisin B1 toxicity were found in the groups fed the uncooked low, mid or high level corn. These effects were markedly reduced in the group fed nixtamalized high level corn and absent, indicating prevention of toxicity, in groups fed the low and mid level nixtamalized corn. Nixtamalization reduced fumonisin B1 by more than 90%. Concentrations were 1.8, 3.6, and 4.2 µg/g in the diets made from uncooked low, mid, and high level corn, respectively, and 0.08, 0.13, and 0.37 µg/g, respectively, in diets prepared from the nixtamalized corn.

In summary, two different but complementary in vivo bioassays demonstrated that the popular alkaline cooking method known as nixtamalization is an effective method for reducing fumonisin concentrations and fumonisin-related toxicity.