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3-deazaadenosine-Induced Disorganization of Macrophage Microfilaments

Carolyn R. Stopford, Gerald Wolberg, Karen L. Prus, Robyn Reynolds-Vaughn and Thomas P. Zimmerman
Proceedings of the National Academy of Sciences of the United States of America
Vol. 82, No. 12 (Jun. 15, 1985), pp. 4060-4064
Stable URL: http://www.jstor.org/stable/26030
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
3-deazaadenosine-Induced Disorganization of Macrophage Microfilaments
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Abstract

3-Deazaadenosine (c3 Ado) has been reported to inhibit a number of cellular functions. These biological effects of c3 Ado have generally been attributed to its ability to act as inhibitor and substrate of S-adenosylhomocysteine hydrolase. In this report, it is revealed by fluorescence microscopy that c3 Ado caused disorganization of the microfilament system of mouse macrophages at concentrations (≥ 5 μ M) similar to those that inhibited antibody-dependent phagocytosis and zymosan-stimulated H2O2 production by these cells. Inhibition of phagocytosis and perturbation of microfilaments by c3 Ado were completely abrogated by washing the macrophages free of this agent and allowing the cells a 30-min recovery period. Furthermore, these effects of c3 Ado on phagocytosis and microfilaments appeared to be independent of the increase in S-adenosylhomocysteine and S-3-deazaadenosylhomocysteine that occurred in these macrophages. First, periodate-oxidized adenosine and 3-deaza(± )aristeromycin, two other inhibitors of S-adenosylhomocysteine hydrolase that caused greater increases in macrophage S-adenosylhomocysteine than did c3 Ado, had no effect on either phagocytosis or microfilaments. Second, pretreatment of macrophages with periodate-oxidized adenosine (to inhibit S-adenosylhomocysteine hydrolase) prevented the subsequent metabolism of c3 Ado to S-3-deazaadenosylhomocysteine but did not diminish the effects of c3 Ado on phagocytosis or microfilaments. These results demonstrate that c3 Ado can perturb the microfilament system of cells and provide an alternative mechanism for the biological effects of c3 Ado.

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