AJCN Cancer Health Disparities Conference
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 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 CAPUTTO, R.
Right arrow Articles by CARPENTER, M. P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by CAPUTTO, R.
Right arrow Articles by CARPENTER, M. P.
Agricola
Right arrow Articles by CAPUTTO, R.
Right arrow Articles by CARPENTER, M. P.

American Journal of Clinical Nutrition, Vol 9, 61-70, Copyright © 1961 by The American Society for Clinical Nutrition, Inc.

The Inhibition of Ascorbic Acid Synthesis by the Process of Lipid Peroxidation in Vitamin E Deficiency

RANWEL CAPUTTO M.D.1, PAUL B. MCCAY PH.D.1, and MARY P. CARPENTER PH.D.1

1 From the Biochemistry Section, Oklahoma Medical Research Institute and Department of Biochemistry, School of Medicine, University of Oklahoma, Oklahoma City, Oklahoma

The mechanism of inhibition of gulonolactone oxidase in liver homogenates from vitamin E deficient rats and rabbits appears to involve the reaction of either an intermediate formed in the enzymic conversion of gulonolactone to ascorbic acid or ascorbic acid itself with a lipid component in the system to produce an inhibitor. The inhibitor or a by-product of its production eventually degradates to yield detectable amounts of malonaldehyde. The action of tocopherol in this sequence would be to prevent the interaction of the postulated intermediate and some component of the tissue lipids.

Although gulonolactone oxidase is inhibited in liver homogenates from vitamin E deficient rats and rabbits, and the inhibition is attributed to lipid peroxidation in the enzyme system, there is, as yet, no direct evidence that a similar phenomenon takes place in vivo. The data show that the usual method for detecting lipid peroxidation in vivo (as defined in this report) would probably give negative results even if such was occurring.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1961 by The American Society for Nutrition