Rat hyperplastic hepatic nodules and primary hepatomas retaining abnormally high pyruvate kinase L type activity.
As reported in our previous paper (Sato et al., Cancer Res., 38: 3086-3093, 1978), most of the hyperplastic hepatic nodules and primary hepatomas induced by N-2-fluorenylacetamide (2-FAA), diethylnitrosamine (DENA), and 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) showed that pyruvate kinase liver (L) type decreases and the prototypic M2 type increases concomitantly with dedifferentiation of tissues. However, at least 14 samples among 120, mostly hyperplastic nodules and highly differentiated hepatomas induced by 2-FAA or DENA, retained exceptionally high activities of the L type, while other enzymes of carbohydrate metabolism in these tissues deviated toward a common pattern similar to that in the fetal liver. Individual patterns of 9 enzymes including pyruvate kinase of carbohydrate metabolism in these samples are arranged and discussed as examples of unbalanced enzyme deviation in hepatocarcinogenesis.
D000818:Animals; D050260:Carbohydrate Metabolism; D002273:Carcinogens; D006528:Carcinoma, Hepatocellular / Q000201:enzymology*; D004588:Electrophoresis, Cellulose Acetate; D006965:Hyperplasia / Q000201:enzymology; D007527:Isoenzymes / Q000378:metabolism*; D008099:Liver / Q000201:enzymology / Q000473:pathology; D008113:Liver Neoplasms / Q000139:chemically induced / Q000201:enzymology*; D008297:Male; D011770:Pyruvate Kinase / Q000378:metabolism*; D051381:Rats
D002273:Carcinogens; D007527:Isoenzymes; D011770:Pyruvate Kinase