Figure 6.
Figure 6. Effects of histamine receptor antagonists and intracellular histamine antagonists on growth of CML cells. (A-B) K562 cells (A) and KU812 cells (B) were incubated in control medium (Co) or in medium containing various concentrations of the HR-1 antagonists loratadine (▪), terfenadine (•), or fexofenadine (▴) at 37°C and 5% CO2 for 48 hours. After incubation, 1 μCi (0.037 MBq) 3H-thymidine was added. Twelve hours later, cells were harvested, and bound radioactivity was measured in a β-counter. Results are expressed as the percentage of Control (Co) and represent the mean ± SD of 3 independent experiments. (C) Primary CML cells obtained from 7 patients (chronic phase, n = 5; accelerated phase, n = 2) were incubated without (Co) or with various concentrations of loratadine as indicated (37°C, 5% CO2) for 48 hours. (D) Primary CML cells obtained from 6 patients (chronic phase, n = 5; accelerated phase, n = 1) were incubated without (Co) or with various concentrations of terfenadine for 48 hours. After incubation, 3H-thymidine uptake was measured. Results are expressed as the percentage of control (Co) and represent the mean ± SD of 7 (C) or 6 (D) independent experiments, respectively. (E) K562 cells and KU812 cells were incubated without (Co) or with various concentrations of N, N-diethyl-2-[4-(phenylmethyl)phenoxy]-ethanamine (DPPE) for 48 hours. After incubation, 3H-thymidine uptake was measured. Results are expressed as the percentage of control (Co) and represent the mean ± SD of 3 independent experiments. (F) Primary CD34+ CML progenitor cells were incubated in control medium (Co) or in medium containing various concentrations of loratadine (•)or terfenadine (▪) at 37°C and 5% CO2 for 48 hours. After incubation, 1 μCi (0.037 MBq) 3H-thymidine was added. Twelve hours later, cells were harvested, and bound radioactivity was measured in a β-counter. Results are expressed as the percentage of control (Co) and represent the mean ± SD of triplicates.

Effects of histamine receptor antagonists and intracellular histamine antagonists on growth of CML cells. (A-B) K562 cells (A) and KU812 cells (B) were incubated in control medium (Co) or in medium containing various concentrations of the HR-1 antagonists loratadine (▪), terfenadine (•), or fexofenadine (▴) at 37°C and 5% CO2 for 48 hours. After incubation, 1 μCi (0.037 MBq) 3H-thymidine was added. Twelve hours later, cells were harvested, and bound radioactivity was measured in a β-counter. Results are expressed as the percentage of Control (Co) and represent the mean ± SD of 3 independent experiments. (C) Primary CML cells obtained from 7 patients (chronic phase, n = 5; accelerated phase, n = 2) were incubated without (Co) or with various concentrations of loratadine as indicated (37°C, 5% CO2) for 48 hours. (D) Primary CML cells obtained from 6 patients (chronic phase, n = 5; accelerated phase, n = 1) were incubated without (Co) or with various concentrations of terfenadine for 48 hours. After incubation, 3H-thymidine uptake was measured. Results are expressed as the percentage of control (Co) and represent the mean ± SD of 7 (C) or 6 (D) independent experiments, respectively. (E) K562 cells and KU812 cells were incubated without (Co) or with various concentrations of N, N-diethyl-2-[4-(phenylmethyl)phenoxy]-ethanamine (DPPE) for 48 hours. After incubation, 3H-thymidine uptake was measured. Results are expressed as the percentage of control (Co) and represent the mean ± SD of 3 independent experiments. (F) Primary CD34+ CML progenitor cells were incubated in control medium (Co) or in medium containing various concentrations of loratadine (•)or terfenadine (▪) at 37°C and 5% CO2 for 48 hours. After incubation, 1 μCi (0.037 MBq) 3H-thymidine was added. Twelve hours later, cells were harvested, and bound radioactivity was measured in a β-counter. Results are expressed as the percentage of control (Co) and represent the mean ± SD of triplicates.

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