Fig. 3.
Fig. 3. Treatment of neutrophils with the NADPH oxidase inhibitor DPI leads to an increase in caspase-3–like activity. Neutrophils undergoing spontaneous or Fas/APO-1–triggered apoptosis (▵ and □, respectively) were cultured in the absence or presence of DPI (10 μmol/L; ▴ and ▪) for various times (0 to 72 hours). Anti-Fas MoAb was used at 250 ng/mL. Determination of AMC release was performed in a fluorometric assay. The maximum rate of AMC release (pmol/min) was estimated by linear regression (r2 > 0.99). The mean and range of duplicate determinations from a representative experiment are shown. Solvent alone (ie, dimethyl sulfoxide [DMSO]) did not affect DEVD-AMC cleavage (data not shown).

Treatment of neutrophils with the NADPH oxidase inhibitor DPI leads to an increase in caspase-3–like activity. Neutrophils undergoing spontaneous or Fas/APO-1–triggered apoptosis (▵ and □, respectively) were cultured in the absence or presence of DPI (10 μmol/L; ▴ and ▪) for various times (0 to 72 hours). Anti-Fas MoAb was used at 250 ng/mL. Determination of AMC release was performed in a fluorometric assay. The maximum rate of AMC release (pmol/min) was estimated by linear regression (r2 > 0.99). The mean and range of duplicate determinations from a representative experiment are shown. Solvent alone (ie, dimethyl sulfoxide [DMSO]) did not affect DEVD-AMC cleavage (data not shown).

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