A number of fungal cultures were screened to select an organism suitable to be used in the detoxification of aflatoxin B1. They were co-cultured in Czapek-Dox-Casamino acid medium with aflatoxin B1 producing Aspergillus flavus. Several fungal cultures were found to prevent synthesis of aflatoxin B1 in liquid culture medium. Among these Phoma sp., Mucor sp., Trichoderma harzianum, Trichoderma sp. 639, Rhizopus sp. 663, Rhizopus sp. 710, Rhizopus sp. 668, Alternaria sp. and some strains belonging to the Sporotrichum group (ADA IV B14(a), ADA SF VI BF (9), strain 720) could inhibit aflatoxin synthesis by > or =90%. A few fungi, namely ADA IV B1, ADA F1, ADA F8, also belonging to the Sporotrichum group, were less efficient than the Phoma sp. The Cladosporium sp. and A. terreus sp. were by far the least efficient, registering <10% inhibition. The cultures which prevent aflatoxin biosynthesis are also capable of degrading the preformed toxin. Among these, Phoma sp. was the most efficient destroying about 99% of aflatoxin B1. The cell free extract of Phoma sp. destroyed nearly 50 microg aflatoxin B1 100 ml(-1) culture medium (90% of the added toxin), and this was more effective than its own culture filtrate over 5 days incubation at 28+/-2 degrees C. The degradation was gradual: 35% at 24 h, 58% at 48 h, 65% at 72 h, 85% at 96 h and 90% at 120 h. The possibility of a heat stable enzymatic activity in the cell free extract of Phoma is proposed.

T 2 toxin (T 2), diacetoxyscirpenol (DAS), fusarenon X (FX) and butenolide (Bd) at concentrations of 0.2, 0.3, 5 and 10 micrograms/site, respectively, were applied individually and in combinations on shaved skin of guinea pigs. Erythema and induration were observed on skin patches treated with the toxins. Increase in the thickness of stratum malpighii was the major histological change observed. Mild to moderate degeneration of fibrocytes and cellular infiltration were found in the corium of skin treated with FX, Bd, DAS and T 2. The order of toxicity of individual toxins was T 2 greater than DAS greater than FX greater than Bd. Combinations of T 2 + FX and T 2 + Bd resulted in antagonism, while DAS + FX and DAS + Bd caused synergism.

Aspergillus niger or Aspergillus tamarii when grown as mixed cultures with toxigenic A. flavus inhibits biosynthesis of aflatoxin by A. flavus, owing primarily to its ability to produce inhibitors of aflatoxin biosynthesis and to their ability to degrade aflatoxin. Gluconic acid partly prevents aflatoxin production. The other factors such as changes in pH of the medium and the effect on the growth of a. flavus have no role in imparting capabilities to these cultures to inhibit aflatoxin production by A. flavus.

A BS TRA CT Peanut, sorghum and maize samples were collected from the wholesale market in Mysore, India, over a period of one year (October 1984 to September 1985). The samples were analysed for the natural occurrence of T-2 toxin (T-2), diacetoxyscirpenol (DAS) and zearalenone by thin-layer chromatography, dermal toxicity test and gas chromatography. Of the total number of peanut samples analysed, 6.9% were positive for the toxic trichothecene(s) (T-2, up to 38.89 mg kg-I; DAS, up to 2.03 mg kg-I); 4.8% of total sorghum samples analysed contained T-2 up to 15 mg kg-I.Zearalenone was not found in any of the samples tested, and no toxins were detected in any of the maize samples. Samples marketed during winter and summer periods were contaminated with the toxins. All the toxin-positive samples except one peanut sample were found in produce stored for more than a week.

Resting cells of Aspergillus flavus synthesized aflatoxin from acetate as the sole carbon source after 36 h of incubation. Addition of pyruvate (5.5 mg/ml) as cosubstrate to [1-'4C]acetate and unlabeled acetate considerably reduced toxin production but increased the radioactivity on the tricarboxylic acid intermediates. This suggests that high tricarboxylic acid activity drastically affected toxin synthesis. '[he carcinogenic property of aflatoxin has stimulated many scientists to study in detail the mode of action, metabolism, and biosynthesis of this toxin. Adye and Mateles (1) have shown the incorporation of labeled carbon from phenylalanine, tyrosine, acetate, and methionine into the toxin molecule. Donkersloot et al. (8), however, excluded the possible involvement of phenylalanine and shikimic acid as biogenetic precursors. Biollaz and co-workers (3) advanced the hypothesis that a polyhydroxy naphthacene and endoperoxy anthraquinone were the intermediates derived from acetate in aflatoxin synthesis. Subsequently, Donkersloot et al. (9) obtained a mutant of Aspergillus parasiticus, with an impaired pathway of aflatoxin biosynthesis, that accumulated averufin, which was shown later by Lin and co-workers to be incorporated into aflatoxin B1 (13). Basappa et al. (2) have shown that acetate is a good precursor for aflatoxin and that kojic acid is not an intermediate in its synthesis. This communication presents some evidence t.o show that the biosynthesis of aflatoxin from acetate follows a route not involving the tricarboxylic acid cycle. MATERIALS AND METHODS All the solvents and chemicals used were of analytical grade. Sodium [1-'4C]acetate was supplied by