NDLI: Experimental studies on the bone metabolism of male rats chronically exposed to cadmium intoxication using dual-energy X-ray absorptiometry.

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Experimental studies on the bone metabolism of male rats chronically exposed to cadmium intoxication using dual-energy X-ray absorptiometry.

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Experimental studies on the bone metabolism of male rats chronically exposed to cadmium intoxication using dual-energy X-ray absorptiometry.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yokota, H. Tonami, H.
Description	Country affiliation: Japan Author Affiliation: Yokota H ( Department of Radiology, Kanazawa Medical University, Uchinada, Kahoku, Ishikawa, Japan. yokota@kanazawa-med.ac.jp)
Abstract	Cadmium (Cd) has been identified as the etiologic agent of itai-itai disease. The purpose of this study was to investigate whether chronic Cd exposure affects bone metabolism in a male rat model and to estimate the bone mineral density (BMD) differences in lumbar and femoral bone because of Cd exposure. Six-week-old male Hos Donryu rats were used in this experiment. Cadmium was administered at a dose of 200 ppm to rats in the diet to produce experimental chronic Cd poisoning. Bone mineral density was measured using dual-energy X-ray absorptiometry (DEXA) with a high-resolution scan collimator (0.25 mm diameter) (Hologic QDR-2000). The Cd content in renal tissue reached a critical concentration of 128.42 +/- 14.38 microg/g 10 months after the administration of the element (Table 3). The average blood urea nitrogen (BUN) value was increased throughout the period of the experiment, and the serum creatinine value of the experimental group showed an increase after 2 months of Cd administration (0.46 +/- 0.09 mg/dL). The concentration of urinary calcium changed in the experimental group after exposure to Cd for 12 months (15.4 +/- 0.13 mg/dL). DEXA showed a greater reduction in the bone mineral density of the 5th vertebral body (L5) in rats that had ingested Cd for 4 months (0.359 +/- 0.013 g/cm2) than in control rats (0.372 +/- 0.012 g/cm2, P < 0.01). On the contrary, the difference in bone mineral content between rats ingesting Cd for 6-8 months and control rats was not significant. However, significant reductions in bone mineral content were again noted in rats that had ingested Cd for 12 months (0.339 +/- 0.023 g/cm2) compared with the control group (0.385 +/- 0.012 g/cm2, P < 0.01). The bone mineral density of the right femoral bone in control rats was 0.328 +/- 0.018 g/cm2 and that in experimental rats was 0.306 +/- 0.012 g/cm2, and a meaningful difference was recognized (P < 0.05). Histological examination of the rats exposed to Cd for 12 months showed that the 5th lumbar vertebral body (L5) exhibited osteomalacia. The results of our studies show that Cd stimulated a loss of bone mineral at an early stage to a great extent in male rats. In the examination of male rats, bone injury and renal functional disorder were encountered simultaneously. This study suggested that osteomalacia was induced by a direct action of Cd on the bone through abnormal calcium homeostasis at an early stage in male rats.
File Format	HTM / HTML
ISSN	07482337
Issue Number	3
Volume Number	24
e-ISSN	14770393
Journal	Toxicology and Industrial Health
Language	English
Publisher	Sage Publications
Publisher Date	2008-04-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Occupational Medicine Discipline Toxicology Bone And Bones Drug Effects Metabolism Cadmium Poisoning Cadmium Toxicity Absorptiometry, Photon Animals Body Weight Bone Density Pathology Administration & Dosage Pharmacokinetics Disease Models, Animal Eating Femur Kidney Lumbar Vertebrae Male Random Allocation Rats Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Public Health, Environmental and Occupational Health Toxicology

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