Dietary protein aflatoxin

Aflatoxin Bi (AFB) is a mold metabolite which has been observed to be acutely toxic and carcinogenic to a wide variety of animals (5,6) and has been implicated in human primary hepatic carcinoma (7, 8). Diets deficient in protein have been reported to increase the susceptibility of mammals to acute AFB toxicity and the induction of cancer (2, 9, 10, 11, 12, 13). Increased dietary proteins have increased the carcinogenic activity of AFB fed to rats (1 4) and trout (15.). Supportive of this latter finding has been the reported direct relationship between dietary protein content and AFB-DNA adduct formation in vivo in rats (16, 17). 

Figure 5. The effect of dietary protein levels on the metabolism of aflatoxin to hydroxylated metabolites. Rats were fed semifurified diets consisting of either 5 casein or 20 casein as the protein source.

The effect of proteins on pollutant toxicity includes both quantitative and qualitative aspects. Experiments show that animals fed proteins of low biological value exhibited a lowered microsomal oxidase activity when dietary proteins were supplemented with tryptophan, the enzyme activity was enhanced. Alteration of xenobiotic metabolism by protein deprivation may lead to enhanced or decreased toxicity, depending on whether metabolites are more or less toxic than the parent compound. For example, rats fed a protein-deficient diet show decreased metabolism but increased mortality with respect to pentobarbital, parathion, malathion, DDT, and toxaphene (Table 6.4). On the other hand, rats treated under the same conditions may show a decreased mortality with respect to heptachlor, CC14, and aflatoxin. It is known that, in the liver, heptachlor is metabolized to epoxide, which is more toxic than heptachlor itself, while CC14 is metabolized to CC13, a highly reactive free radical. As for aflatoxin, the decreased mortality is due to reduced binding of its metabolites to DNA. 

Van Herwaarden, A.E., Wagenaar, E., Kamekamp, B., Merino, G., Jonker, J.W. Schinkel, A.H. (2006) Breast cancer resistance protein (Brcp1/Abcg2) reduced systemic exposure of the dietary carcinogens aflatoxin B1, IQ and Trp-P-1 but also mediates their secretion into breast milk. Carcinogenesis 27,123-130. 

Toxic compounds polychlorinated biphenyls, polycyclic aromatic hydrocarbons, organochlorine pesticides, chlorinated pesticides, dioxins, veterinary drug residues, hormone residues, aflatoxins, toxic compounds in shellfish. Compoimds of nutritional significance in foods vitamins, fat, lipids, carbohydrates, protein, energy-calorific value, proximates, dietary fibre, ash. Other compounds hormones in blood serum... 

The carcinogenicity of aflatoxin is reduced by protein deficiency, presumably because of reduced metabolic activation to the epoxide intermediate which may be the ultimate carcinogen which binds to DNA (figure 5,26). A deficiency in dietary fatty acids also decreases the activity of the microsomal enzymes. Thus, ethylmorphine, hexobarbital and aniline metabolism are decreased, possibly because lipid is required for cytochromes P-450. Thus, a deficiency of essential fatty acids leads to a decline in both cytochromes P-450 levels and activity in vivo. 

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