Study on clinical chemistry and DNA ploidy pattern changes in carcinogenesis of the rat liver and kidney

간과 선장의 암유발과정에서 혈액화학효소 및 DNA ploidy pattern 의 변화에 대한 조사

This study was carried out to investigate on the serum chemistry and the DNA ploidy changes in carcinogenesis of the rat liver and kidney. Sixty male Sprague-Dawley rats were divided into two groups. Group I was non-treated control. Group II was given initiators (2,2'-dihydroxy- di-N-propylnitrosamine, 0.1% in drinking water(d.w.) for 1 week and N-ethyl-N-hydroxy-ethylnitrosamine; 0.15% in d.w. for 1 week) and promoters (3'methyl-cholanthrene; 3'MC, l0mg/kg, intraperitoneally(i.p.) twice a week and DL-serine; 0.05% in d.w. for 5 weeks, from 3 to 8 weeks). All examinations were performed at 12 and 20 weeks RBC, HGBCp＜0.05) and PCVCp＜0.01) significantly decreased in Group II at 20 weeks. Activities of ALT, AST(p＜0.05) and GGT(p＜0.01) were significantly increased in Group II at 20 weeks. Flow cytometric analysis showed hepatocyte nuclei from normal livers were predominantly tetraploid(66~67%) and then diploid(28~30%). Most of hepatocyte nuclei from carcinogen-treated rats were diploid (52~68%) and less were tetraploid(28~42%). Neoplastic liver nodules and hepatocellular carcinoma contained almost exclusively diploid nuclei. Renal cell nuclei from normal kidney were predominantly diploid(88~93%), those from carcinogen-treated rats had an abnormal DNA-content peak(aneuploidy, 6-7%), near the tetraploidy area. These results suggest that diploidy may be an effective screening marker of the liver carcinogenesis. Aneuploidy may be an useful marker in assessment of the experimental renal carcinogenesis.