Acute Harmful Effects after Single Intravenous Dose of Cadmium Fluoride in Rats (Second report)-Changes of cadmium and fluoride excretion in bile and urine-

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  • Adachi Kazuya
    Department of Hygiene and Public Health, Osaka Medical College
  • Dote Tomotaro
    Department of Hygiene and Public Health, Osaka Medical College
  • Yamadori Emi
    Department of Hygiene and Public Health, Osaka Medical College
  • Mitsui Go
    Department of Hygiene and Public Health, Osaka Medical College
  • Kono Koichi
    Department of Hygiene and Public Health, Osaka Medical College

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Other Title
  • フッ化カドミウム静脈内単回投与後の急性有害影響（第２報）―カドミウムおよびフッ素の胆汁および尿中排出量の経時的変化―
  • フッカ カドミウム ジョウミャクナイ タンカイ トウヨゴ ノ キュウセイ ユウガイ エイキョウ ダイ 2ホウ カドミウム オヨビ フッソ ノ タンジュウ オヨビ ニョウチュウ ハイシュツリョウ ノ ケイジテキ ヘンカ
  • -Changes of cadmium and fluoride excretion in bile and urine-
  • -カドミウムおよびフッ素の胆汁および尿中排出量の経時的変化-

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Abstract

Cadmium fluoride(CdF2)have been recently used for electronics device in industrial fields. In previous study, we investigated the dose-effect relationships of acute toxicities from the standpoint of occupational health. It would be strongly influenced by metabolism of CdF2. Therefore, this study was designed to investigate the early dynamic state of Cd and F in bile and urine after the acute exposure of CdF2. Rats were received a single intravenous injection of saline or CdF2(1.34, 2.67, or 4.01 mg/kg)which were the same doses of the previous study. Bile was collected at intervals of 30 min until 300 min. Urine was collected for 300 min. Volume of bile and urine were decreased in CdF2 treated groups. Total biliary Cd was excreted in the 2.67 and 4.01 group much more than 1.34 group. The peaks of maximum excretion were 30-60 min in the 2.67 group and 60-90 min in the 4.01 group respectively. Our previous study indicated that CdF2 caused severe liver dysfunction at a dose of 2.67 and 4.01 mg/kg and proximal tubular damage at a dose of 4.01 mg/kg. Abnormalities in Cd kinetics could be resulted from extensive hepatic damage at a toxic dose. The differences of kinetics would be caused by the saturation of the accumulation capacity of the liver. Although biliary ionized F(F)was dose-relatedly excreted, urinary F did not show dose-related excretion. Therefore, the metabolism of F was mainly disordered by renal dysfunction rather than hepatic damage. The toxicity of CdF2 may be enhanced by kinetics abnormalities caused by liver and kidneys dysfunctions.

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