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Benzodiazepine-induced superoxide signalsB cell apoptosis: mechanistic insight and potential therapeutic utility
Neal B. Blatt, … , Anthony W. Opipari Jr., Gary D. Glick
Neal B. Blatt, … , Anthony W. Opipari Jr., Gary D. Glick
Published October 15, 2002
Citation Information: J Clin Invest. 2002;110(8):1123-1132. https://doi.org/10.1172/JCI16029.
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Categories: Article Autoimmunity

Benzodiazepine-induced superoxide signalsB cell apoptosis: mechanistic insight and potential therapeutic utility

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Abstract

Research Article

Authors

Neal B. Blatt, Jeffrey J. Bednarski, Roscoe E. Warner, Francesco Leonetti, Kathryn M. Johnson, Anthony Boitano, Raymond Yung, Bruce C. Richardson, Kent J. Johnson, Jonathan A. Ellman, Anthony W. Opipari Jr., Gary D. Glick

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Figure 1

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(a) Structure of Bz-423 and inactive congeners. (b) Effect of Bz-423, 4′...
(a) Structure of Bz-423 and inactive congeners. (b) Effect of Bz-423, 4′-chlorodiazepam (4-ClDz), PK11195, ΔNAP, and ΔOH on Ramos cell viability at 24 hours, determined by PI permeability. The ED50 of Bz-423 is 4 μM. (c) Interference contrast micrographs (×400) of cells treated for 24 hours with vehicle, Bz-423 (10 μM), or Bz-423 (10 μM) plus z-VAD (100 μM). (d) After treatment as in c, cells were analyzed by flow cytometry to detect DNA content; percentages indicate fraction of cells with hypodiploid (apoptotic) DNA. Distribution of nonapoptotic cells in G1, S, and G2/M phases was altered by Bz-423 (33%, 42%, and 24% for control vs. 53%, 38%, and 8% for Bz-423). Pretreatment with z-VAD blocked formation of hypodiploid DNA and partially restored cell cycle distribution. All panels are representative of more than five separate determinations.
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