Induction of lipid peroxidation in mice by hexavalent chromium and its relation to the toxicity.
- 1 January 1989
- journal article
- research article
- Published by Japanese Society of Veterinary Science in The Japanese Journal of Veterinary Science
- Vol. 51 (6) , 1103-1110
- https://doi.org/10.1292/jvms1939.51.1103
Abstract
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 20 mg 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 lifer 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, indicating of the kidney damage, observed at 24 hr after injection of Cr(VI) were inhibited by simultaneous injection of 100 mg/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-.rho.-phenylenediamine (DPPD), and 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 peroxidation in the liver and kidney of the mice, while lipid peroxidation is not responsible for the tissue damage induced by Cr(VI).This publication has 4 references indexed in Scilit:
- Experimental bases for ascorbic acid therapy of poisoning by hexavalent chromium compoundsInternationales Archiv für Arbeitsmedizin, 1984
- Glutathione depletion and in vitro lipid peroxidation in mercury or maleate induced acute renal failureBiochemical Pharmacology, 1983
- Cadmium toxicity and lipid peroxidation in isolated rat hepatocytesToxicology and Applied Pharmacology, 1980
- Chromate metabolism in liver microsomesBiological Trace Element Research, 1979