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. Author manuscript; available in PMC: 2014 May 14.
Published in final edited form as: Arthritis Rheum. 2002 Jan;46(1):175–190. doi: 10.1002/1529-0131(200201)46:1<175::AID-ART10015>3.0.CO;2-H

Figure 4.

Figure 4

Effect of H2O2 treatment on the production of reactive oxygen intermediates (ROIs) in SLE patients. A, ROI levels were monitored in live cells by flow cytometry after staining with annexin V–phycoerythrin (PE; FL-2) and dihydrorhodamine (DHR; FL-1) (dot-plots). Numbers in the upper right corner of the dot-plots show the percentage of annexin V–positive cells; numbers at the top of the first row of histograms show the mean channel fluorescence of DHR (FL-1) in annexin V–negative cells. Histograms of H2O2-treated cells (shaded) are overlaid on those of untreated control cells (open). ROI production was also monitored by hydroethidine (HE) staining. Numbers at the top of the second row of histograms show the mean channel fluorescence of HE-positive cells (FL-2) gated on annexin V–FITC-negative cells (FL-1). B, Correlation between H2O2-induced ROI production and apoptosis, as determined by Pearson's correlation coefficient. Increases in apoptosis and ROI production were estimated by annexin V positivity (Δannexin V) and DHR fluorescence (ΔDHR), respectively. C, H2O2-induced ROI production in SLE patients and controls. Bars show the mean ± SEM of H2O2-induced changes in DHR and HE fluorescence in PBLs from SLE patients and controls. See Figure 1 for other definitions.