Ammoniation of aflatoxin-containing corn: distribution, in vivo covalent deoxyribonucleic acid binding, and mutagenicity of reaction products

Abstract

3H]Aflatoxin B1 (AF ' B,) was ammoniated at 100 OC and the isolated aflatoxin D1 (AFD,) characterized by 'H NMR and mass spectrometry. AFDl was found to be 130-fold less mutagenic than AFB, in the Ames test. In vivo covalent binding to rat liver DNA expressed in the units of a covalent binding index (CBI, a quantitative indicator for genotoxicity) of [14C]AFDl was below the detection limit of 71 and at least 280-times lower than for AFB1, although AFD, still has the 8,9a double bond. After ammoniation of [14C]AFB1-spiked corn grits for 34 days (18.8% H20/2.02% NH3, 25 "C), 14C distribution and CBI were measured: 7% of the radioactivity was CH2C12 extractable but 14% was extractable when acidified prior to extraction. The H 2 0 phase contained 42% 14C with a CBI of 1000 but only 31% 14C with a CBI of below the detection limit of 145 when acidified prior to extraction. The extracted corn had still a radioactivity of 33% (38% respectively) with a CBI of <126. More than 85% of the H20 fraction pass a dialpis membrane with an exclusion limit of 14 OOO dalt~ns. The results indicate that ammoniation reduces the genotoxicity of AFB,-containing corn at least 20 times. Besides unreacted AFBl the aqueous phase contained about 7% of a still toxic AFBl hydrolysis product, which can rebuild AFBl after acidification.Numerous attempts have been made to detoxify by chemical means natural goods contaminated with aflatoxins (Codifer et al.

Effect of citric acid supplemented diets on aflatoxin degradation, growth performance and serum parameters in broiler chickens

“…It also suggests that the molecule structure in post-treated aflatoxin contaminated samples changes, the lactone ring may be opened. Thus, detoxification initially involves the formation of the b-keto acid structure (catalyzed by de acidic medium), followed by hydrolysis of the lactone ring yielding the AFD 1 molecule, derivated from decarboxylation of the lactone ring-opened form of AFB 1 (Méndez-Albores et al 2005), which is 130 times less mutagenic in the Ames test and presenting 20-fold toxicity decrease (Schroeder et al 1985). Therefore, the fluorescence strength varies in the HPLC chromatograms at the same retention time values.…”

Genotoxicity testing of extracts from aflatoxin-contaminated peanut meal, following chemical decontamination

“…The disadvantage of the high sensitivity of the assays for a¯atoxin B 1 itself, is the fact that the presence of even low levels of the mycotoxin may obscure the eOE ects of weaker genotoxic AFB 1 degradation products and that the genotoxic potency of a compound does not necessarily correlate with its carcinogenic potency. For example, AFD 1 , the product resulting from the ammoniation of pure a¯atoxin B 1 , has been reported to be 100± 450 times less mutagenic in the Salmonella/microsome test than the parent compound (Lee et al 1981, Schroeder et al 1985. Therefore, it is essential to test the degradation products in the absence of the original a¯atoxins.…”

“…AFD 1 was shown to possess mutagenic properties, although to a lesser extent than the parent compound (Schroeder et al 1985). In the case of decontaminated feedstuOE s, however, these compounds appear to represent at best only a very minor fraction of the degraded a¯atoxin B 1 and most compounds appear to be bound to feed components (Lee and Cucullu 1978, Lee et al 1979, Grove et al 1984, Park 1984, Schroeder et al 1985, Martinez et al 1994.…”

“…In the case of pure a¯atoxin B 1 , a number of ammoniation products have been identi® ed, among them a¯atoxin D 1 and compounds with molecular weights of 236, 206 and lower (Lee et al 1974, 1984, Cucullu et al 1976, Schroeder et al 1985. AFD 1 was shown to possess mutagenic properties, although to a lesser extent than the parent compound (Schroeder et al 1985).…”

“…AFD 1 was shown to possess mutagenic properties, although to a lesser extent than the parent compound (Schroeder et al 1985). In the case of decontaminated feedstuOE s, however, these compounds appear to represent at best only a very minor fraction of the degraded a¯atoxin B 1 and most compounds appear to be bound to feed components (Lee and Cucullu 1978, Lee et al 1979, Grove et al 1984, Park 1984, Schroeder et al 1985, Martinez et al 1994. Toxicological studies with trout and rats con® rm the decreased toxicity of the decontaminated products but in general lack the sensitivity to prove the safety of the products (Brekke et al 1977, Norred and Morrisey 1983, Frayssinet and LafargeFrayssinet 1990, Bailey et al 1994.…”