Abstract
Carcinogenic/toxic effects of ochratoxin A (OTA) in various internal organs of Plymouth Rock chicks were determined. The number of OTA-induced neoplasms was similar in chicks given 25 ppm L-β-phenylalanine (PHE) in addition to 5 ppm OTA compared to chicks given only 5 ppm OTA, which showed that PHE cannot be used as a real protector against the carcinogenic or toxic effects of OTA in chicks. OTA was found to provoke strong degenerative changes in liver and kidneys, degenerative changes and depletion of cells in lymphoid organs, oedematous and degenerative changes in the brain, muscular haemorrhages and fatty changes in the bone marrow. The target organs for carcinogenic effect of OTA in chicks were found to be kidneys and liver.
Highlights
Ochratoxin A (OTA) is a mycotoxin widely encountered in animal feeds and human foods
Some authors suggest that part of the toxic effect of OTA is due to the structural homology with phenylalanine (PHE), resulting in an inhibition of protein synthesis due to a competition for the specific t-RNA [10,11]
The most obvious clinical signs as weakness or dullness, goose plumage, transient diarrhoea and growth depression were seen in all chicks from the groups treated with OTA, but the same were less pronounced in chicks supplemented with PHE
Summary
Ochratoxin A (OTA) is a mycotoxin widely encountered in animal feeds and human foods. The most obvious effects of OTA-contaminated feed on chicks are reported to be reduced rates of weight gain [1,2,3], decreased egg production [4], immunosuppressive effects [2] and increased mortality [5]. There are many other reports on various carcinogenic effects of OTA, but in these attention is usually focussed on mice or rats [6,7,8] and there is a lack of evidence with regard to carcinogenic effects of OTA on chicks. Haazele et al [4] reported that ascorbic acid supplementation in laying hen diets can partially reduce the toxic effects of nephrotoxic mycotoxin OTA. Some authors suggest that part of the toxic effect of OTA is due to the structural homology with phenylalanine (PHE), resulting in an inhibition of protein synthesis due to a competition for the specific t-RNA [10,11]
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