Journal of Animal Science, Vol 70, Issue 12 3968-3988, Copyright © 1992 by American Society of Animal Science

JOURNAL ARTICLE

A review of recent advances in understanding ochratoxicosis

R. R. Marquardt and A. A. Frohlich
Department of Animal Science, University of Manitoba, Winnipeg, Canada.

Ochratoxin A (OA) is a toxin that contains an isocoumarin moiety linked by a peptide bond to phenylalanine. It is produced by certain Penicillium (mainly P. verrucosum) and Aspergillus (mainly A. alutaceus) species of storage fungi. Total amounts of OA and other related toxins produced by these fungi are influenced by many factors. Several forms of OA have been discovered, some of which are highly toxic, whereas others have lower toxicity. Ochratoxin A has been detected in foods, feeds, animal tissues, and human blood in both Europe and North America. It has been implicated in the fatal human disease Balkan endemic nephropathy, has been shown to be a powerful carcinogen in rodents, and produces many other adverse effects in animals. It is absorbed passively throughout the gastrointestinal tract and in an active manner in the kidney. It is subjected to intestinal secretion and reabsorption via enterohepatic recycling. Binding of OA in the blood to the albumin fraction and recycling in the bile and kidney contributes to its long half-life in animals. Ochratoxin A is hydrolyzed to its nontoxic alpha form (O alpha) by microorganisms in the rumen, cecum, and large intestine. The toxin is excreted primarily in the urine as O alpha and to a lesser degree as OA; smaller amounts of OA and O alpha are generally excreted in the feces. Three distinct mechanisms of OA toxicity have been proposed; other toxic effects of OA seem to be secondary in nature. Several different strategies can be employed for controlling or neutralizing the effect of OA, including the use of proper storage conditions, the use of specific adsorbents to reduce absorption of OA, and the feeding OA-contaminated feedstuffs to ruminants. Antioxidants such as ascorbic acid have been shown to reduce the toxic effects of OA in laying hens. In summary, OA contamination of cereal food and feed may occur, given appropriate conditions. Implementation of suitable procedures may eliminate or minimize this potentially serious problem.

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