AJP - GI Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Gastrointest Liver Physiol 264: G1009-G1015, 1993;
0193-1857/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jourd'Heuil, D.
Right arrow Articles by Meddings, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jourd'Heuil, D.
Right arrow Articles by Meddings, J. B.

AJP - Gastrointestinal and Liver Physiology, Vol 264, Issue 6 1009-G1015, Copyright © 1993 by American Physiological Society


ARTICLES

Lipid peroxidation of the brush-border membrane: membrane physical properties and glucose transport

D. Jourd'Heuil, P. Vaananen and J. B. Meddings
Gastrointestinal Research Group, Faculty of Medicine, University of Calgary, Alberta, Canada.

During inflammatory conditions, peroxidation of biological membranes often takes place. Deleterious physiological consequences, in terms of membrane function, could theoretically be mediated by either direct oxidative attack upon integral membrane proteins or by indirectly altering the lipid environment surrounding these proteins. To address this issue, in vitro peroxidation of guinea pig brush-border membrane vesicles was induced by incubation of the vesicles with ferrous sulfate and ascorbic acid. We found that ongoing peroxidative attack initiates lipid peroxidation and radically alters the physical properties of the membrane lipid bilayer in a well-defined and regional manner. Peroxidation of microvillous membrane produced an increasingly rigid membrane. Coupled with these alterations was a fivefold reduction in maximal rates of sodium-dependent glucose transport that appeared to have a multifactorial origin. Approximately one-third of this reduction was secondary to altered membrane physical properties and was reversible by fluidizing the vesicles and returning membrane physical properties to normal. The remaining reduction in glucose transport activity was not responsive to membrane fluidization and was presumably related to direct damage of the transport protein.


This article has been cited by other articles:


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
F. Courtois, I. Suc, C. Garofalo, M. Ledoux, E. Seidman, and E. Levy
Iron-ascorbate alters the efficiency of Caco-2 cells to assemble and secrete lipoproteins
Am J Physiol Gastrointest Liver Physiol, July 1, 2000; 279(1): G12 - G19.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
A. Ismaili, J. B. Meddings, S. Ratnam, and P. M. Sherman
Modulation of host cell membrane fluidity: a novel mechanism for preventing bacterial adhesion
Am J Physiol Gastrointest Liver Physiol, July 1, 1999; 277(1): G201 - G208.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
B. M. Chung, J. K. Wong, J. A. Hardin, and D. G. Gall
Role of actin in EGF-induced alterations in enterocyte SGLT1 expression
Am J Physiol Gastrointest Liver Physiol, February 1, 1999; 276(2): G463 - G469.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. L. Bates, K. A. Sharkey, and J. B. Meddings
Vagal involvement in dietary regulation of nutrient transport
Am J Physiol Gastrointest Liver Physiol, March 1, 1998; 274(3): G552 - G560.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online