Induction of lipid peroxidation in mice by hexavalent chromium and its relation to the toxicity.

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  • 6価クロムによるマウスの生体内脂質過酸化促進と毒性との関係
  • 6価クロムによるマウスの生体内脂質過酸化促進と毒性との関係〔英文〕
  • 6カ クロム ニ ヨル マウス ノ セイタイナイ シシツ カサンカ ソクシン

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Comparative effects of hexavalent (K2Cr2O7: Cr(VI)) and trivalent chromium (Cr(NO3)3: Cr(III)) on the development of lipid peroxidation, and the relationship between the lipid peroxidation and damage to tissues were studied using male ddY strain mice. The animals were administered with either of two chemicals at a dose of 20mg Cr/kg by a single intraperitoneal injection. The results obtained were as follows: (1) Lipid peroxidation in the liver, as measured by the synthesis of thiobarbituric acid reactive substances (TBARS), showed a significant increase at 24 and 48 hr after Cr(VI) injection, while in the kidney it was observed only at 48 hr. In the mice administered with Cr(III), TBARS formation in the liver went down below the control levels, while no change was observed in the kidney. (2) Chromium contents in the liver and kidney showed a maximum level at 6 hr after injection of Cr(VI) and then those declined to the half of the maximum level at 48hr, respectively. Chromium contents in the liver and kidney of the mice injected with Cr(III) were lower than those injected with Cr(VI) during the experimental period. (3) Increases of TBARS formation in the liver, chromium content in the liver and kidney, and ornithine carbamyl transferase (OCT) activity indicative of the liver cell damage, and urea nitrogen content in the serum, indicative of the kidney damage, observed at 24 hr after injection of Cr(VI) were inhibited by simultaneous injection of 100mg/kg of L-ascorbic acid, as antichrome agent, respectively. These observations might suggest a possible causative role of lipid peroxidation in Cr(VI) toxicity. (4) Incremental formation of TBARS in the liver after Cr(VI) injection was inhibited by simultaneous injection of N, N-diphenyl-p-phenylenediamine (DPPD), an antioxidant, but DPPD did not suppress the increase of chromium content of the organs examined (the liver and kidney), serum OCT activity and urea nitrogen content observed after Cr(VI) injection. This finding contradicted with the conclusion described above. The results of this study confirmed Cr(VI) induces lipid peroxidatioin in the liver and kidney of the mice, while lipid peroxidation is not responsible for the tissue damage induced by Cr(VI)

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