help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
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 Okayasu, T.
Right arrow Articles by Farber, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Okayasu, T.
Right arrow Articles by Farber, J. L.

American Journal of Pathology, Vol 117, 163-166, Copyright © 1984 by American Society for Investigative Pathology


REGULAR ARTICLES

Cytochalasin delays but does not prevent cell death from anoxia

T Okayasu, MT Curtis and JL Farber

The role of alterations in the cytoskeleton in the anoxic death of cultured hepatocytes was evaluated with the use of cytochalasin B and colchicine. The addition of 50 microM Cytochalasin did, however, reduce the rate of accumulation of dead cells but was without effect on the number of cells that died. After 6 hours of anoxia in the presence of cytochalasin, 80% of the cells were dead. The same number of cells were dead after 4 hours in the absence of cytochalasin. Colchicine was without effect on the cell killing by anoxia. Cytochalasin also did not prevent the increase in the molecular order of the membranes of the anoxic hepatocytes as determined by electron spin resonance spectroscopy. In the presence or absence of cytochalasin, anoxia increased the order parameter, S, of hepatocytes spin-labeled with 12- doxyl stearic acid. These data indicate that changes in the organization of microfilaments that can be prevented by cytochalasin may aggravate the mechanisms mediating the anoxic death of the hepatocytes, but such mechanisms are essentially independent of these alterations in the cytoskeleton. The data do not exclude from a role in anoxic cell death other cytoskeletal changes that may not be affected by either cytochalasin or colchicine.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1984 by the American Society for Investigative Pathology.