Abstract
Aflatoxin B1 (AFB1) exerts a chronic carcinogenic and an acute toxic effect on animals. Whereas the mechanism for carcinogenicity is known, no mechanism has been proposed for the toxic action. Among the most prominent signs of aflatoxicosis in several species, including birds and mammals, are hypolipidaemia, hypocholesterolaemia, and hypocarotenaemia, associated with severe hepatic steatosis and weight loss. We suggest that these signs of acute imbalance of lipid metabolism can be the result of the chemical modification (blocking) of key lysyl residues on the LDL protein B-100 by the activated AFB1 molecule. Modified LDLs are not recognised by their specific receptors and thus are rejected by peripheral cells. Upon return to the liver, the modified particles bind to the sinusoidal lining cells. Lipid starvation of peripheral tissues takes place while fat accumulates in the liver. This abnormal state is maintained and reinforced by further modification of nascent apoproteins, which in turn become unable to receive a lipid load for as long as aflatoxin continues to be available in the liver.
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