摘要
Gap junctional intercellular communication (GJIC) as measured by metabolic cooperation was examined in a rat glioma cell line P_(98)F_(47). X-ray induced mutants of P_(98)F_(47) cells were grown in 6-thioguanine selective medium (6TG medium) to separate 6TG-resistant HGPRT- mutant cells (6TG^r). By co-culturing 200 6TG^r cells with varied high densities of the wild type 6TG-sensitive cells (6TG^s), it was found that the recovery of 6TG^r cells depended on the density of 6TG^s cells. Higher densities of 6TG^s cells reduced the recovery of 6TG^r cells. These results demonstrate the ability of P_(98)F_(47) cells to perform metabolic cooperation which is indicative of GJIC. When metabolic cooperation was inhibited, increased recovery of 6TG^r cells was observed. Presented results also demonstrate metabolic cooperation between P_(98)F_(47) glioma cells and normal rat glial cells. Effect of tumor promoting chemicals on metabolic cooperation of P_(98)F_(47) cells was studied.~3H-uridine nucleot de echnique was used to confirm the above observations. The results suggest that these cells may provide the basis for an in uitro assay specially to study brain tumor promoters and neurotoxins.
Gap junctional intercellular communication (GJIC) as measured by metabolic cooperation was examined in a rat glioma cell line P<sub>98</sub>F<sub>47</sub>. X-ray induced mutants of P<sub>98</sub>F<sub>47</sub> cells were grown in 6-thioguanine selective medium (6TG medium) to separate 6TG-resistant HGPRT- mutant cells (6TG<sup>r</sup>). By co-culturing 200 6TG<sup>r</sup> cells with varied high densities of the wild type 6TG-sensitive cells (6TG<sup>s</sup>), it was found that the recovery of 6TG<sup>r</sup> cells depended on the density of 6TG<sup>s</sup> cells. Higher densities of 6TG<sup>s</sup> cells reduced the recovery of 6TG<sup>r</sup> cells. These results demonstrate the ability of P<sub>98</sub>F<sub>47</sub> cells to perform metabolic cooperation which is indicative of GJIC. When metabolic cooperation was inhibited, increased recovery of 6TG<sup>r</sup> cells was observed. Presented results also demonstrate metabolic cooperation between P<sub>98</sub>F<sub>47</sub> glioma cells and normal rat glial cells. Effect of tumor promoting chemicals on metabolic cooperation of P<sub>98</sub>F<sub>47</sub> cells was studied.<sup>3</sup>H-uridine nucleot de echnique