Influence of Chronic Exposure to Carbon Monoxide on the Kidney Histopathological and Biochemical Study

Park, Jong Chul

Abstract

Influence of chronic exposure to carbon monoxide on the kidney of white rats has been studied histopathologically and biochemically and the following results were obtained: Experimental animals were devided as. 1) C1, control (non-exposure group); 6 rats 2) C2; acute exposure to 0.5% carbon monoxide until death; 10 rats 3) E1; chronic exposure to 0.05% carbon monoxide for 8 weeks; 6 rats 4) E2; chronic exposure to 0.05% carbon monoxide for 4 weeks; 6 rats 5) E3; acute poisoning with 0.5% carbon monoxide until death after with 0.05% carbon monoxide for 8 weeks; 5 rats 6) E4; acute exposure to 0.5% carbon monoxide until death after chronic exposure to 0.05% carbon monoxide for 4 weeks; 5 rats 1. All experimental groups except the acute exposure have increased tendency of total lactic acid dehydrogenase(LDH) activities of the kidney tissue. The most significant increase was observed in the chronic 8 weeks group (E1). 2. The patterns of LDH isoenzyme activity of the control group were as LDH1>LDH2> LDH5.>.LDH4>LDH3 and those of the chronic 8 weeks group were as LDH1>LDH5>LDH4> LDH2>LDH3. 3. Activities of LDH, and LDH, decreased and those of..LDH4 and LDH5 increased in chronic exposure, but no change was observed in the acute exposure group. 4. The chronic 8 weeks group had more change in LDH isoenzyme activity than in the chronic 4 weeks group. Change in LDH isoenzyme band was most significant in LDH5 of the chronic 8 weeks group. 5. Acclimation or increase of tolerance was noticed in chronic long term exposure with low concentration of carbon monoxide. G. In the acute exposure group, moderate degree of diffuse congestion, hemorrhage and edema was observed in the kidney tissue. Scattered glomerular atrophy was also observed throughout the chronic 8 weeks group and glomerular hyalnization and fibrosis were occasionally observed. 7. Actuate exposure coupled with chronic exposure for 8 weeks caused more marked tubular atrophy. cortical hemorrhage and glomerular fibrosis.