الفهرس 
Introd uctionOnly 14 pages are availabe for public view
 |  | from | 112 |  |  |
| | | from | 112 | | |
Abstract
In actuality, the metabolism of lead in bone cells can not be viewed independently of lead metabolism in the mineral bone matrix. Movement of lead into bone is predominantly mediated by osteoblasts activity, while osteoclast activity is mainly responsible for loss of lead from bone. It is important to note that lead readily displaces Ca 2+by cation exchange proceesses in the hydroxyapatite crystal in both natural and synthetic apatite.(Marcus, 1985) The first characterizations of bone lead metabolism in vitro were conducted using bone organ cultures of fetal rat radius and ulna. These studies showed that at least one compartment of total bone lead was readily exchanged & was modulated by the same ions & hormones that regulate bone calcium metabolism. (Rosen, 1985) The toxicity of lead in the skeleton is like that produced in other target tissues in that lead does not cause a unique disease or pathological lesion, but rather decrementalloss of organ function manifested by many biochemical, molecular, and structural lesions. The effects of lead on the skeleton may be produced through two general processes. First, effects may be indirect and secondary to lead effects on the endocrine organs which synthesize or produce hormones regulating bone function and bone mineral metabolism. Second, lead may direct perturb bone cell function by: A) Producing overt toxicity and cell death in bone cells.