The cellular and molecular toxicity of lead in primary and clonal osteoblastic bone cells

Miscellaneous · Sun Jan 01 00:00:00 EST 1989

OSTI ID:6703681

Long, G J

First, steady state kinetic models of lead metabolism and calcium homeostasis were developed in both primary and clonal osteoblastic bone cells. Secondly, the effect of lead on cellular calcium homeostasis was determined. Finally, the effect of lead on 1,25 (OH){sub 2}D{sub 3} induced production of osteocalcin, a protein synthesized and secreted by osteoblasts, was investigated. Lead metabolism in osteoblastic bone cells was characterized by three intracellular pools. The largest of these, S{sub 3}, included mitochondrial lead and accounted for 70 percent of total cell lead in primary osteoblastic bone cells and 85 percent of total lead in clonal osteoblastic bone cells. None of the kinetic pools were saturated at lead concentrations up to 100 {mu}M lead. Calcium homeostasis in osteoblastic bone cells was also described by a three compartment, intracellular kinetic model.

• Research Organization: Arkansas Univ., Fayetteville, AR (USA)
• OSTI ID: 6703681
• Resource Relation: Other Information: Thesis (Ph. D.)
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
CALCIUM
HOMEOSTASIS
LEAD
TOXICITY
PROTEINS
BIOSYNTHESIS
BONE CELLS
METABOLISM
MITOCHONDRIA
ALKALINE EARTH METALS
ANIMAL CELLS
CELL CONSTITUENTS
CONNECTIVE TISSUE CELLS
ELEMENTS
METALS
ORGANIC COMPOUNDS
ORGANOIDS
SOMATIC CELLS
SYNTHESIS
560300* - Chemicals Metabolism & Toxicology