Abstract
An overview is presented of studies on effects of Cd on (1) female mice during pregnancy and lactation and after ovariectomy and (2) bone organ/cell culture systems. The gastrointestinal absorption of Cd increased two- to threefold in mouse dams during pregnancy and lactation, with both the kidneys and duodenum of the dam showing striking increases in Cd deposition. Dietary Cd at 5 or 50 μg g−1 caused a dose-dependent decrease in femur Ca content in multiparous mouse dams but not in nonpregnant controls. In addition, dietary Cd at 50 μg g−1 significantly increased the loss of bone mineral that occurs normally in mice after removal of the ovaries. In cultures of fetal rat limb bones prelabeled with 45Ca, Cd at 10 nM (1 ng g−1) caused a release of 70% of the 45Ca, similar to the release caused by 10 nM parathyroid hormone. This level of Cd also caused a fivefold increase in the number of multinucleated osteoclast-like cells formed during in vitro incubation of progenitor-enriched mononuclear bone marrow cells. These results support the view that Cd exposure contributed to the pathogenesis of Itai-Itai disease among multiparous, postmenopausal women in Japan and provide evidence that Cd may act directly on bone.
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Bhattacharyya, M.H. Cadmium-induced bone loss: Increased susceptibility in females. Water Air Soil Pollut 57, 665–673 (1991). https://doi.org/10.1007/BF00282930
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DOI: https://doi.org/10.1007/BF00282930