Fig. 2.
Inhibition of chemotherapeutic drug-induced apoptosis by the ICE inhibitor zVAD in different cell lines. CEM and SHEP cells were incubated with 100 μg/mL CR (circles), 100 ng/mL DX (triangles), and 100 μg/mL MX (squares) in the presence or absence of the ICE protease inhibitor zVAD (Enzyme Systems Products, Dublin, CA). Apoptosis was measured as described in Fig 1. SHEP (A) or CEM cells (B) were cotreated with drugs and various concentrations of the inhibitor for 40 or 30 hours, respectively. (C) Effect of delayed addition of zVAD on drug-induced apoptosis in CEM cells. Cells were treated with drugs for 34 hours and then analyzed for cell death. The addition of zVAD (60 μmol/L) was delayed for the indicated time. Data represent the mean ± SD from four experiments with duplicate measurements. Spontaneous apoptosis was less than 10%. The percentage of living cells after 34 hours of drug treatment without the inhibitor was less than 5% for each drug.

Inhibition of chemotherapeutic drug-induced apoptosis by the ICE inhibitor zVAD in different cell lines. CEM and SHEP cells were incubated with 100 μg/mL CR (circles), 100 ng/mL DX (triangles), and 100 μg/mL MX (squares) in the presence or absence of the ICE protease inhibitor zVAD (Enzyme Systems Products, Dublin, CA). Apoptosis was measured as described in Fig 1. SHEP (A) or CEM cells (B) were cotreated with drugs and various concentrations of the inhibitor for 40 or 30 hours, respectively. (C) Effect of delayed addition of zVAD on drug-induced apoptosis in CEM cells. Cells were treated with drugs for 34 hours and then analyzed for cell death. The addition of zVAD (60 μmol/L) was delayed for the indicated time. Data represent the mean ± SD from four experiments with duplicate measurements. Spontaneous apoptosis was less than 10%. The percentage of living cells after 34 hours of drug treatment without the inhibitor was less than 5% for each drug.

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