Histidine endogenous production

Phytic acid and camosine (histidine-containing dipeptide), obtained from cereal and meat by-products, are effective inhibitors of hpid oxidation by several mechanisms, including metal inactivation and free radical quenching. Uric acid obtained from the decomposition of adenosine triphosphate in muscle also inhibits lipid oxidation by the same mechanisms. However, the importance of uric acid as an endogenous antioxidant in muscle foods is not clear. Various protein concentrates from soybeans, cottonseed and peanuts inhibit hpid oxidation in muscle foods. In addition to their iron binding activity, these crade extracts contain complex polyphenolic flavonoids that have potent antioxidant activity. 

HNE-Modified Protein This arises by the covalent binding of HNE, an endogenously generated major lipid peroxidation product derived from breakdown of lipids containing u)-6 fatty acids (lin-oleic and arachidonic acid), to nucleophilic sites in the given protein. HNE reacts with the side chains of cysteine (Cys, C), histidine (His, H), and lysine (Lys, K) in an order of reactivity Cys His > Lys. 

Decarboxylation of amino-acids under normal circumstances—e.g. of tyrosine, tryptophane, histidine—represents a very small part of their metabolism. Thus the endogenous serotonin production in man may be estimated at 10-20 mg per 24 hr " compared with a daily intake of 500-1000 mg tryptophane in the food. This represents the decarboxylation of only 1-2% of the amino-acid for the formation of amines. A similar rate of production is assumed for tryptamine, which also originates from trypto-phane. Changes which arise in pathological conditions will be considered in the section concerning amine-metabolism and when discussing the amine-producing tumors. 

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