Figure 2.
Figure 2. CER generation and SM hydrolysis in B cells. (Ai) Rituximab induces CER generation and SM hydrolysis in B cells. Daudi (□) and RL (▪) cells were prelabeled with [9, 10-3H] palmitic acid or [methyl-3H]choline to equilibrium for 48 hours and then treated with 10 μg/mL rituximab for various time points. After which, both tritiated CER (top line) and SM (bottom line) levels were quantitated as described in “Materials and methods.” Results are representative of 3 independent experiments. (Aii) Mean of peak CER levels obtained from 3 independent experiments. *P < .01. (B) Effect of fumonisin B1 on cell viability. Daudi cells were preincubated (•) or not (○, □) 24 hours with 25 μM fumonisin B1 and then treated (○, •) or not (□) with 10 μg/mL rituximab. Cell number was estimated by trypan blue exclusion assay. Results are the mean of 3 independent experiments ± SD.

CER generation and SM hydrolysis in B cells. (Ai) Rituximab induces CER generation and SM hydrolysis in B cells. Daudi (□) and RL (▪) cells were prelabeled with [9, 10-3H] palmitic acid or [methyl-3H]choline to equilibrium for 48 hours and then treated with 10 μg/mL rituximab for various time points. After which, both tritiated CER (top line) and SM (bottom line) levels were quantitated as described in “Materials and methods.” Results are representative of 3 independent experiments. (Aii) Mean of peak CER levels obtained from 3 independent experiments. *P < .01. (B) Effect of fumonisin B1 on cell viability. Daudi cells were preincubated (•) or not (○, □) 24 hours with 25 μM fumonisin B1 and then treated (○, •) or not (□) with 10 μg/mL rituximab. Cell number was estimated by trypan blue exclusion assay. Results are the mean of 3 independent experiments ± SD.

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