“…In contrast, OTA in cereals in warmer climatic zones such as tropical regions is primarily produced by A. ochraceus (Krogh ). The natural occurrence of OTA in cereal grains and livestock feed is widespread (Dwivedi & Burns ).…”
An experiment was conducted to investigate the influence of repeated ingestion of ochratoxin A (OTA) on milk production of lactating Holstein cows over 28 days, and the carry-over of OTA from the diets into the milk and tissues of the cows. Nine cows were divided into three groups, labeled OTA5, OTA50 and OTA100, and fed a diet containing 5, 50 and 100 µg OTA/kg of dry matter, respectively. Body weight, feed intake and daily milk yield in cows were not different among the three groups during the OTA-intake period. OTA residues were neither detected in the tissues, such as liver, kidney, muscles, fat and jejunoileum, nor in the milk of any cows in the OTA intake groups. In contrast, a small amount of OTA (0.1 µg/kg) was detected in the blood plasma of one sample in the OTA50 group and multiple samples in the OTA100 group. The results of this study show that the ingestion of diets containing up to 100 µg/kg of OTA over 28 days does not affect feed intake or milk production of cows, and the dietary OTA is not carried over into milk and edible tissues such as the liver, muscles and fat.
“…In contrast, OTA in cereals in warmer climatic zones such as tropical regions is primarily produced by A. ochraceus (Krogh ). The natural occurrence of OTA in cereal grains and livestock feed is widespread (Dwivedi & Burns ).…”
An experiment was conducted to investigate the influence of repeated ingestion of ochratoxin A (OTA) on milk production of lactating Holstein cows over 28 days, and the carry-over of OTA from the diets into the milk and tissues of the cows. Nine cows were divided into three groups, labeled OTA5, OTA50 and OTA100, and fed a diet containing 5, 50 and 100 µg OTA/kg of dry matter, respectively. Body weight, feed intake and daily milk yield in cows were not different among the three groups during the OTA-intake period. OTA residues were neither detected in the tissues, such as liver, kidney, muscles, fat and jejunoileum, nor in the milk of any cows in the OTA intake groups. In contrast, a small amount of OTA (0.1 µg/kg) was detected in the blood plasma of one sample in the OTA50 group and multiple samples in the OTA100 group. The results of this study show that the ingestion of diets containing up to 100 µg/kg of OTA over 28 days does not affect feed intake or milk production of cows, and the dietary OTA is not carried over into milk and edible tissues such as the liver, muscles and fat.
“…Ochratoxin A (OTA) is a secondary metabolite of some toxigenic storage fungal species of the genera Aspergillus and Penicillium [ 1 , 2 ]. It has a widespread occurrence in foods and feedstuffs [ 3 ], e.g., in Canada, Denmark, Germany, Sweden and United Kingdom [ 4 ]. In tropical and subtropical areas OTA is mainly produced by Aspergillus species (mainly A. ochraceus ) whereas in temperate regions Penicillium species are of great importance, especially P. verrucosum [ 1 ].…”
Ruminants are much less sensitive to ochratoxin A (OTA) than non-ruminants. The ruminal microbes, with protozoa being a central group, degrade the mycotoxin extensively, with disappearance half lives of 0.6–3.8 h. However, in some studies OTA was detected systemically when using sensitive analytical methods, probably due to some rumen bypass at proportions of estimated 2–6.5% of dosage (maximum 10%). High concentrate proportions and high feeding levels are dietary factors promoting the likeliness of systemic occurrence due to factors like shifts in microbial population and higher contamination potential. Among risk scenarios for ruminants, chronic intoxication represents the most relevant.
“…of OA and its metabolites; its biochemical mechanism of action; the degree to which humans are exposed to the toxin; and means by which the toxic effects of OA can be reduced. Several reviews have been published on different aspects of OA (Chu, 1974; Cole and Cox, 1981; Roschenthaler et al, 1984;Steyn, 1984; Schaeffer and Hamilton, 1986; Burns and Dwivedi, 1988; Dwivedi and Burns, 1988;Kuiper-Goodman, 1990; Marquardt et al, 1990;Pestka and Bondy, 19901.…”
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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