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用二乙基亚硝胺（ＤＥＮ）诱发大鼠肝癌，隔周测定肝脏胞液、膜性和胞核中的蛋白激酶Ａ（ＰＫＡ）和蛋白激酶Ｃ（ＰＫＣ）的活力。发现胞液ＰＫＡ在诱癌过程中活力改变不大，胞液ＰＫＣ则逐步增高，在第１３周和２０周形成两个活力高峰。膜性ＰＫＡ和ＰＫＣ都呈双相变化，即在癌前期（１０－１４周）增加，癌形成期（１７－２０周）反而降至正常以下，胞核ＰＫＡ和ＰＫＣ也都在癌前期升至高峰，而癌形成期则低于癌前期，但仍高于正常（ＰＫＡ）或接近正常（ＰＫＣ）。因只有膜性ＰＫＣ在大鼠老化时降低，故这些变化不是鼠龄变化的结果，而是ＤＥＮ诱癌所引起，其变化机理可能与下降调节、细胞内转位或两型同工酶相反的升降变化有关。
Rat liver cancer was induced with diethylnitrosamine (DEN) and the activity of protein kinase A (PKA) and protein kinase C (PKC) in the cytosol, membranous and nucleus of hepatocytes was determined every other week. It was found that the cytosolic PKA did not change its activity during the process of carcinogenesis and the cytosolic PKC gradually increased, forming two peaks of activity at the 13th and 20th weeks. Membrane PKA and PKC showed biphasic changes, that is, in the precancerous phase (10-14 weeks) increased, the cancer formation phase (17-20 weeks) instead fell below normal, nucleus PKA and PKC also rose to precancerous The peak, while the cancer formation phase is lower than the precancerous phase, but still higher than normal (PKA) or near normal (PKC). Because only membranous PKC is reduced during aging in rats, these changes are not the result of age-dependent changes in mice, but are caused by DEN-induced cancer, and their mechanisms of change may be inversely related to downregulation, intracellular translocation, or both types of isoenzymes. Changes related to lift.