Cellular lead toxicity and metabolism in primary and clonal osteoblastic bone cells

Journal Article · Thu Feb 01 00:00:00 EST 1990 · Toxicology and Applied Pharmacology; (USA)

DOI:https://doi.org/10.1016/0041-008X(90)90032-P· OSTI ID:6936012

Long, G J; Rosen, J F; Pounds, J G ^[1]

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1. Brookhaven National Laboratory, Upton, NY (USA)

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 {sup 210}Pb 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 {sup 210}Pb as 5 microM lead acetate for 20 hr, and kinetic parameters were determined by measuring the efflux of {sup 210}Pb from the cells over a {sup 210}-min period. The intracellular metabolism of {sup 210}Pb was characterized by three kinetic pools of {sup 210}Pb in both cell types. Although the values of these parameters differed between the primary osteoblastic cells and ROS cells, the profile of {sup 210}Pb 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.

• OSTI ID: 6936012
• Journal Information: Toxicology and Applied Pharmacology; (USA), Vol. 102:2; ISSN 0041-008X
• Country of Publication: United States
• Language: English

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63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
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TOXICITY
BONE CELLS
CLONE CELLS
EGTA
LACTATE DEHYDROGENASE
LEAD 210
METABOLISM
MICE
MITOCHONDRIA
OSTEOSARCOMAS
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SURVIVAL TIME
TISSUE DISTRIBUTION
TRACER TECHNIQUES
TUMOR CELLS
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ALPHA DECAY RADIOISOTOPES
ANIMAL CELLS
ANIMALS
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
CARBOXYLIC ACIDS
CELL CONSTITUENTS
CELL CULTURES
CHELATING AGENTS
CONNECTIVE TISSUE CELLS
DISEASES
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ELEMENTS
ENZYMES
EVEN-EVEN NUCLEI
GLYCOLS
HEAVY NUCLEI
HEMIACETAL DEHYDROGENASES
HYDROXY COMPOUNDS
ISOTOPE APPLICATIONS
ISOTOPES
LEAD ISOTOPES
MAMMALS
METALS
NEOPLASMS
NUCLEI
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANOIDS
OXIDOREDUCTASES
OXYGEN COMPOUNDS
PHOSPHORUS COMPOUNDS
RADIOISOTOPES
RODENTS
SARCOMAS
SKELETAL DISEASES
SOMATIC CELLS
VERTEBRATES
YEARS LIVING RADIOISOTOPES
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