Gastrointestinal urease in man ' Part I Activity of mucosal urease

The relationship postulated between hepatic coma and hyperammonaemia implicates the gastrointestinal tract as a major source of the excess ammonia in the peripheral blood of some patients with cirrhosis (Butt and Summerskill, 1961; Chalmers, 1960; Sherlock, Summerskill, White, and Phear, 1954). Conventional therapy, comprising protein restriction, antibiotics, and enemas, is directed toward eliminating from the gut nitrogenous material and bacteria (Butt and Summerskill, 1961; Chalmers, 1960; Sherlock et al., 1954) from which ammonia and other toxic substances may be produced. The metabolic processes involving ammonia in the gastrointestinal tract ofman are poorly defined (Chalmers, 1960; McDermott, Adams, and Riddell, 1954); ammonia can be produced in the stomach (FitzGerald and Murphy, 1950), while both secretion and absorption have been quantitated in the small intestine (Ewe and Summerskill, 1965). Several enzymes capable of liberating ammonia from various substrates occur in the bacterial flora of the gut and may also be present in the mucosa; they include oxidative deaminases, dehydrases, combined transaminase-deamidases, and urease (Bessman, 1956; White, Handler, and Smith, 1964). Urease, which produces ammonia by hydrolysis of urea, may originate from either the mucosa or the bacterial flora of the gut in animals (Conway, FitzGerald, McGeeney, and Geoghegan, 1959; Dintzis and Hastings, 1953; Kornberg and Davies, 1955; Kornberg, Davies, and Wood, 1954); findings in man pertaining to mucosal urease activity are scanty (FitzGerald and Murphy, 1950; Fossel, 1948)