I would like to ask the experts (especially chemists) who have studied the chemical properties of trichothecenes: Does ammoniation have any effect on trichothecenes (T-2 toxin, DON, satratoxin etc.)? Can ammonia detoxify trichothecenes at least to some extent, or is ammonia completely inert when mixed with trichothecene mycotoxins (i.e. no chemical reaction)?
I have reviewed the scientific literature and I cant find any information on this. Ammoniation is mentioned (and in some countries used) for detoxification of aflatoxins, but there is absolutely no information on what happens when trichothecenes are mixed with ammonia.
Ammoniation has been used to decontaminate aflatoxin from corn, cottonseed, cottonseed meal and peanut meal. The ammoniation steps are as follows: rehydrate the grain or ingredient to 12 to 16% moisture and then treat either with anhydrous ammonia gas or ammonium hydroxide (aqua ammonia) under high temperature and high pressure (HT/HP). During this procedure, hydrated ammonia attacks Aflatoxin B1 lactone ring followed by decarboxylation to chemically inactive form. There are same practical limitations for this method such as ammonia is highly volatile and corrosive. Safety hazard may be one of the reasons why it is not used commonly around the world. Unlike aflatoxins, trichothecene mycotoxins have trichothecene ring which may not be susceptible to the action of ammonia. As per my knowledge I have not come across any work on ammoniation and trichothecene mycotoxins. Hope this helps. Regards,
Dr. Swamy Haladi Alltech Canada
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Branislav Despotov
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23 de febrero de 2009
Thank you Swami Haladi,
I know that Aflatoxin B1 can be detoxified with ammonia, and I think the technique you explained is still used in some countries. The main question is: Does any detoxification happen when trichothecene mycotoxins are mixed with ammonia?
In the meantime I found two studies (albeit the first one is not directly related to mycotoxins in food) which state somewhat condtradictory information about this issue:
1) Indoor Mold, Toxigenic Fungi, and Stachybotrys chartarum: Infectious Disease Perspective
http://cmr.asm.org/cgi/content/full/16/1/144
From this study, the following quote pertains to my question:
Trichothecenes resist sunlight, UV light, X-rays, heat (up to 120°C), and acids. They are readily destroyed by alkali, which allows for detoxification with sodium, potassium, calcium, or ammonium hydroxide or gaseous ammonia (28, 336). This has important ramifications for building remediation.
The references for this assertion are:
28. Bakai, S. M. 1960. In V. I. Bilai (ed.), Mycotoxicosis of man and agricultural animals, p. 163-167. Izd. Akad. Nauk Ukr. S.S.R., Kiev, USSR.
336. Poliakov, A. A. 1948. Rukovodstvo po Veterinarnoi Dezinfeksii, p. 154-158. Ogiz-Selskhozgiz, Moscow, USSR.
These are rather old Russian studies, so I dont know if something new has been found regarding this issue in the meantime.
The other study that mentions effect of ammonia on trichothecenes is:
2) In Vitro Metabolism of T-2 Toxin, ROBERT A. ELLISON AND FRANK N. KOTSONIS, School of Pharmacy, University of Wisconsin, Madison, Wisconsin 53706, 1973
http://aem.asm.org/cgi/reprint/27/2/423.pdf
From this study:
Incubation of T-2 toxin with the 9,000 x g supernatant fluid of human liver resulted in the appearance on TLC of a new, more polar product after 10 min. Isolation and characterization of this compound by proton magnetic resonance and mass spectrometry as well as TLC comparison in four solvent systems showed it to be identical with HT-2 toxin (reference 1
see Fig. 1). By TLC analysis, the half-life of T-2 toxin in this system was found to be 20 4 5 min. This metabolite could not be produced by incubation with cofactors alone or by incubation with cofactors in the presence of blood expressed from the liver. Thus, production of HT-2 is most likely due to a liver esterase. This enzyme cleaves the same acetyl group which can be selectively removed by treatment of T-2 toxin with aqueous ammonia (10). Excess material obtained during the extraction procedure did not interfere with TLC analysis, and HT-2 toxin could be recovered in 84% yield after chromatography. Under the same conditions, bovine liver also produced HT-2 toxin but more slowly. The half-life of T-2 toxin in this system was found to be 40 5 min.
So according to the second study, T-2 toxin was transformed by the liver enzyme esterase into HT-2 toxin, and the same result can be obtained with aqueous ammonia. Therefore, it follows that T-2 toxin can be transformed into HT-2 toxin with aqueous ammonia. It is not clear whether HT-2 toxin is only an intermediate or the final product of this chemical reaction. If it is the final, then ammonia doesnt detoxify T-2 toxin completely. If it is an intermediate product, what happens next, if the ammoniation continues?
Could somebody shed some more light on this problem?
Regards.
