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Relationship between osteoid formation and iron deposition induced by chronic cadmium exposure in ovariectomized rats
Author(s) -
Wako Yumi,
Hiratsuka Hideaki,
Kurotaki Tetsurou,
Tsuchitani Minoru,
Umemura Takashi
Publication year - 2021
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.4118
Subject(s) - osteoid , ovariectomized rat , osteomalacia , anemia , endocrinology , medicine , pathogenesis , deposition (geology) , erythropoietin , lesion , deferoxamine , fibrosis , chemistry , osteoporosis , pathology , estrogen , biology , paleontology , sediment
Abstract Itai‐itai (Japanese, “It hurts! It hurts!”) disease (IID), a form of osteomalacia, can be induced in ovariectomized rats by long‐term administration of cadmium (Cd). This IID rat model shows severe anemia, severe nephropathy, and osteomalacia accompanied by iron (Fe) deposition at the mineralization front. We characterized the pathogenesis of Cd‐induced bone lesions by investigating the relationship between Fe deposition and osteoid tissue formation in ovariectomized rats. The rats were injected with CdCl 2 (0.5 mg/kg) for 70 weeks, with or without co‐injection of erythropoietin (EPO) for varying lengths of time to elucidate whether EPO prevents and/or cures anemia, and, with the restoration from anemia, lessens the osteoid tissue formation. Necropsies were performed at 25, 50, or 70 weeks. Fe deposition at the mineralization front of bone was found at 50 weeks and increased thereafter. Animals injected with EPO showed decreased Fe deposition, although there was no relation between EPO administration and osteoid formation in the femur. Because the increase in bone lesion severity was independent of the amount of Fe deposition, we suggest that Fe deposition is not involved in the etiology of Cd‐induced femoral bone lesions.