lead-radioisotopes and Osteosarcoma

A knowledge of bone lead metabolism is critical for understanding the toxicological importance of bone lead, as a toxicant both to bone cells and to soft tissues of the body, as lead is mobilized from large reservoirs in hard tissues. To further understand the processes that mediate metabolism of lead in bone, it is necessary to determine lead metabolism at the cellular level. Experiments were conducted to determine the intracellular steady-state 210Pb kinetics in cultures of primary and clonal osteoblastic bone cells. Osteoblastic bone cells obtained by sequential collagenase digestion of mouse calvaria or rat osteosarcoma (ROS 17/2.8) cells were labeled with 210Pb as 5 microM lead acetate for 20 hr, and kinetic parameters were determined by measuring the efflux of 210Pb from the cells over a 210-min period. The intracellular metabolism of 210Pb was characterized by three kinetic pools of 210Pb in both cell types. Although the values of these parameters differed between the primary osteoblastic cells and ROS cells, the profile of 210Pb was remarkably similar in both cell types. Both types exhibited one large, slowly exchanging pool (S3), indicative of mitochondrial lead. These data show that primary osteoblastic bone cells and ROS cells exhibit similar steady-state lead kinetics, and intracellular lead distribution. These data also establish a working model of lead kinetics in osteoblastic bone cells and now permit an integrated view of lead kinetics in bone.

Topics: Animals; Cell Survival; Clone Cells; Egtazic Acid; Kinetics; L-Lactate Dehydrogenase; Lead; Lead Radioisotopes; Mice; Mitochondria; Osteoblasts; Osteosarcoma; Phosphates; Rats; Tumor Cells, Cultured