Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Appl Physiol 51: 1477-1483, 1981;
8750-7587/81 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
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 Wright, J. R.
Right arrow Articles by Miles, P. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wright, J. R.
Right arrow Articles by Miles, P. R.

Journal of Applied Physiology, Vol 51, Issue 6 1477-1483, Copyright © 1981 by American Physiological Society


ARTICLES

Ascorbate uptake by isolated rat lung cells

J. R. Wright, V. Castranova, H. D. Colby and P. R. Miles

Experiments were done to determine the intracellular concentration of ascorbate in isolated rat lung cells and the concentration in plasma and to study ascorbate influx in these cells. The intracellular ascorbate concentration was 2.25 mM and the plasma level was about 0.14 mM; i.e., the lung cell ascorbate concentration was about 16 times greater than the plasma level. When the cells were incubated in medium containing physiological levels of ascorbate (0.1 mM), influx increased linearly up to 60 min of incubation and was 0.54 +/- 0.04 nmol.10(7) cells-1.h-1. Influx was dependent on the extracellular ascorbate concentration. At concentrations ranging from 0.025 to 1 mM, uptake appeared to exhibit saturation kinetics with an apparent Km of 0.16 mM. At physiological levels of extracellular ascorbate (0.1 mM) at least 90% of the uptake appeared to be carrier mediated, and this influx was inhibited by various metabolic inhibitors. In addition, ascorbate influx was inhibited by ouabain and removal of extracellular sodium. These results suggest that lung cells contain a transport mechanism for ascorbate that is energy-dependent and that may be coupled to Na+ influx.


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
S. C. Rumsey, O. Kwon, G. W. Xu, C. F. Burant, I. Simpson, and M. Levine
Glucose Transporter Isoforms GLUT1 and GLUT3 Transport Dehydroascorbic Acid
J. Biol. Chem., July 25, 1997; 272(30): 18982 - 18989.
[Abstract] [Full Text] [PDF]




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