Fumonisins are
mycotoxins produced by Fusarium verticillioides. They are toxic to animals and exert their effects through mechanisms involving disruption of
sphingolipid metabolism.
Fumonisins are converted to their hydrolyzed analogs by alkaline cooking (nixtamalization). Both
fumonisins and hydrolyzed
fumonisins are found in nixtamalized foods such as tortillas, and consumption of tortillas has been implicated as a risk factor for
neural tube defects (NTD).
Fumonisin B(1) (FB(1)) induced NTD when given (ip) to pregnant LM/Bc mice; however, neither the NTD induction potential of hydrolyzed
fumonisin B(1) (HFB(1)) nor its affect on
sphingolipid metabolism in pregnant mice have been reported. The teratogenic potential of FB(1) and HFB(1) was therefore compared using the LM/Bc mouse model. Dams were dosed (ip) with 2.5, 5.0, 10, or 20 mg/kg (< or = 49 micromol/kg)
body weight (bw) HFB(1) on embryonic day (E)7-E8. Negative and positive control groups were given vehicle or 10 mg/kg (14 micromol/kg) bw FB(1), respectively. The high dose of HFB(1) disrupted
sphingolipid metabolism, albeit slightly, but did not cause maternal liver lesions or NTD (n = 8-10 litters per group). In contrast, 10 mg/kg bw FB(1) markedly disrupted maternal
sphingolipid metabolism, caused hepatic apoptosis in the dams, increased
fetal death rates, and decreased
fetal weights. Furthermore, NTD were found in all FB(1)-exposed litters (n = 10), and 66 +/- 24% of the fetuses were affected. The findings indicate that HFB(1) does not cause NTD in the sensitive LM/Bc mouse model and only weakly disrupts
sphingolipid metabolism at doses up to sevenfold higher (micromole per kilogram
body weight basis) than the previously reported lowest observed adverse effect level for FB(1).