This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Montaudon, D. Articles by Robert, J. Search for Related Content PubMed PubMed Citation Articles by Montaudon, D. Articles by Robert, J.

Fluorescence Anisotropy of Cell Membranes of Doxorubicin-sensitive and -resistant Rodent Tumoral Cells¹

Laboratoire de Biochimie, Université de Bordeaux II, 146 rue Léo Saignat [D. M., J. R.], Laboratoire de Biochimie, Fondation Bergonié, 180 rue de Saint-Genés [P. V., J. R.], and INSERM U.117, 229 cours de l'Argonne [D. L-G.], 33076 Bordeaux Cédex, France

We have studied the plasma membrane fluidity of rat C6 glioblastoma cells and simian virus 40-transformed mouse liver cells in culture that had been rendered resistant to doxorubicin. This was done by the evaluation of fluorescence anisotropy of two probes; diphenylhexatriene was used on membrane microsomal fractions, and trimethylammonium-diphenylhexatriene was used on whole cell suspensions as a plasma membrane-specific probe since it does not enter the cells. A higher degree of membrane fluidity was exhibited with both techniques by doxorubicin-resistant glioblastoma cells as compared to the doxorubicin-sensitive strain, but in the transformed liver cells no such alteration was seen in the physical properties of their plasma membranes. A higher degree of acyl group unsaturation was noticed in the glioblastoma cells but not in the transformed liver cells upon acquisition of doxorubicin resistance. A similar simultaneous increase in acyl group unsaturation and membrane fluidity can be obtained easily by growing the sensitive cells with a medium supplemented with exogenous polyunsaturated fatty acids. This alteration does not modify the sensitivity of the cells to doxorubicin. We conclude from our work that the increase in membrane fluidity, which is frequently associated with drug resistance, is neither necessary nor sufficient for the expression of the resistance. The reason for a link between cell resistance to doxorubicin and plasma membrane fluidity remains to be found.

¹ This work was supported by grants from the Fédération Nationale des Centres de Lutte contre le Cancer.

² To whom requests for reprints should be addressed.

Received 3/20/86. Revised 7/ 7/86. Accepted 8/ 4/86.

This article has been cited by other articles:

				J. P. Robinson and R.W. Pfeifer New Technologies for Use in Toxicology Studies: Monitoring the Effects of Xenobiotics on Immune Function International Journal of Toxicology, May 1, 1990; 9(3): 303 - 317. [Abstract] [PDF]