AJCN North Carolina Research Campus
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by SPECTOR, I.
Right arrow Articles by METZ, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by SPECTOR, I.
Right arrow Articles by METZ, J.
Agricola
Right arrow Articles by SPECTOR, I.
Right arrow Articles by METZ, J.

American Journal of Clinical Nutrition, Vol 21, 1374-1380, Copyright © 1968 by The American Society for Clinical Nutrition, Inc.

Resistance of Liver Formiminoglutamic Acid Transferase to Experimental Protein Malnutrition in Weanling Rats

I. SPECTOR M.D.1 and J. METZ M.D., M.C. PATH.1

1 From The South African Institute for Medical Research, Johannesburg, South Africa

Histidase, urocanase, and formiminoglutamic acid transferase, three enzymes necessary for the degradation of histidine to glutamic acid, have been assayed in the livers of weanling rats given a maize diet. The enzymes showed different sensitivity to the effect of the maize diet. Histidase activity was moderately reduced, urocanase markedly diminished, whereas the specific activity of FIGLU transferase remained similar to that of control animals. Enzyme activity rapidly returned to normal following refeeding with stock diet.

Although rats given maize showed normal FIGLU transferase activity in the liver, excessive FIGLU excretion occurred even in the absence of histidine loading. This excessive FIGLU excretion did not occur when the liver concentrations of both folate and vitamin B12 were maintained.

The reduction in histidase and urocanase activities was not related to folate or vitamin B12 deficiency per se. The diminution of urocanase activity was associated with excessive urocanicaciduria only when the pathway was stressed by administration of a histidine load, and this urocanicaciduria could be prevented by PGA supplementation, despite persistently diminished liver urocanase activity.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1968 by The American Society for Nutrition