M. A. Bennett
Dec 1, 1950
Citations
1
Influential Citations
41
Citations
Journal
The Journal of biological chemistry
Abstract
It has been shown in this laboratory that rats bred on our preexperimental food will grow on a synthetic diet in which homocystine is the Drily sulfur-containing amino acid and which contains no known sources of ‘labile methyl” groups (1, 2). The ability to utilize homocystine is eventually lost on the synthetic diet, probably due to the exhaustion of stored ‘actors involved in homocystine metabolism. However, this ability to utilize homocystine can be restored by supplementation of the diet with iver extract Lilly (LEL). The liver preparation represents the antianemia lraction formerly called Cohn fraction G (2). In order to find out whether the antianemia principle in the LEL is the active agent in the utilization Df homocystine, two Lederle preparations were also fed to rats on a homocystine-synthetic diet containing 2 per cent sulfasuxidine. One preparation, liver extract parenteral (Lederle), is similar to LEL, the other, Lederle concentrated solution of liver extract, is a product derived from the preceding preparation low in folic acid but 4 to 5 times as high in antianemia potency. Although the liver extract parenteral gave a growth response rimilar to that of LEL when given both orally and by intramuscular ine&ion, the concentrated solution of liver extract gave negative results with both methods of administration (2). It was assumed from these results that the component of the liver preparations active in the utilization of homocystine was not identical with the antianemia principle, although its distribution parallels that of the latter to some degree. Since this original work was published, crystalline folic acid and vitamin Blz have become available. When the previously cited experiments were carried out, 2 per cent sulfasuxidine was added to the basal diet to inhibit possible bacterial synthesis of factors involved in the utilization of homo:ystine. At that time, ryzamin-B was our source of folic acid and the ntestinal synthesis of additional amounts was inhibited by the sulfasuxiline. Recently some observations were made on the r81e of crystalline