Unique toxic effects may be precipitated on feeding excess quantities of individual amino acids by virtue of their particular structural or functional properties. Benevenga and Steele (1984) reviewed the evidence derived principally from observations with laboratory animals. The acute growth depressions caused by excesses of some individual amino acids may be accompanied by profound and specific lesions in organs and tissues. Toxicities may also be demonstrated in farm livestock, and Baker (1989) indicated that, at 40 g kg"1 diet, methionine is the most growth-depressing amino acid. At this inclusion level, leucine, isoleucine, and valine do not impair growth when added to practical diets for pigs and poultry. Excess threonine depresses growth in chicks but not in pigs, whereas arginine is more toxic to the pig than the fowl. Scherer and Baker (2000) suggest that excess methionine may increase vitamin B6 requirements of young chicks. In calves, manifestations of methionine toxicity include reduced food intake, depressed N retention and body weight loss (Abe et ai, 1999). Such instances of toxicity are, in the main, confined to experimental situations. However, Adeola and Ball (1992) reported that dietary excesses of tryptophan or tyrosine administered for 5 days prior to slaughter reduced stress in pigs, a response attributed to increased hypothalamic concentrations of several neurotransmitters.
Of some practical significance is the occasional incidence, under natural conditions, of interstitial pulmonary emphysema and oedema in ruminants subjected to sudden changes in diet. This syndrome is associated with the ruminal production of abnormal quantities of 3-methylindole (skatole) from tryptophan. Oral or intraruminal administration of tryptophan or the indole to cattle can cause respiratory distress and pulmonary lesions similar to those seen in the natural disorder (Carlson et ai, 1968). Toxicity is mediated after the indole is metabolically activated by a mixed function oxidase to a reactive free radical product capable of initiating tissue damage in the lung. The severity of the syndrome may be reduced by dietary treatments which increase tissue glutathione. Tryptophan toxicity depends on the balance between metabolic activation of 3-methylindole and its conjugation with glutathione.
The unusual amino acid, lysinoalanine, may arise during alkali treatment of protein feedstuffs (Finot, 1983). The feeding of proteins containing lysinoalanine causes a reduction in biological values of diets for rats and in the induction of renal lesions. The significance of these observations in farm animal nutrition requires elucidation since alkali treatment may be used for denaturing antigenically active globular proteins in soybean meal.
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