Liver arginase activity as related to blood urea in acute uremia of new-born rats.

There is evidence to indicate that the demands imposed upon the mammalian organism to metabolize protein may be reflected by changes in the arginase activity of the liver. Particularly those conditions leading to a stimulation of protein catabolism, with its concomitant increase in the formation of urea, frequently elicit a corresponding increase in the arginase activity of the liver. Thus, elevations in liver arginase activity have been observed under the dietary influence of fasting (1, 2), increased levels of protein intake (3, 4), and thiamine deficiency (5). Hormonal secretions, known to control the rate of gluconeogenesis, effect a rise in the arginase content of the liver when injected into hypophysectomized or adrenalectomized animals (6-9). Previous reports from this laboratory have described a high incidence of early mortality of rats born to mothers maintained on rations composed mainly of crude or purified plant materials (10-12). A characteristic feature of the syndrome which preceded death, referred to as “acute uremia of the new-born,” was the very high level of urea in the blood. The subcutaneous administration of vitamin Blz shortly after birth was effective in preventing the onset of the uremic syndrome. If this uremic condition actually reflects an increased rate of nitrogen catabolism which can be prevented by vitamin B12, it appeared possible that, under such circumstances, the arginase activity of the liver might be increased in order to accommodate the need for this enzyme. In the present paper data are reported on the relationship between argihase activity of the liver and the concentration of urea in the blood of normal and uremic young rats.