Furihata C, Kodama K, Matsushima T
J Natl Cancer Inst. 1981 Nov;67(5):1101-4.
Changes in pepsinogen isoenzyme patterns were examined in the pyloric mucosae of the stomachs of noninbred male Wistar rats after short-term administration of gastric carcinogens. N-Methyl-N-nitro-N-nitrosoquanidine, N-ethyl-N1-nitro-N-nitrosoguanidine, and N-propyl-N-nitro-N-nitrosoguanidine, which induce stomach cancer in rats, decreased the content of pepsinogen isoenzyme 1 )Pg 1), which was separated by poly-acrylamide gel electrophoresis. They also decreased the pepsingoen content of the pyloric mucosa. 4-Nitroguinoline 1-oxide, which induces a low incidence of stomach cancer in rats, rarely decreased the Pg 1 content or the pepsinogen content of the pyloric mucosa, and the incidence of such decreases was not statistically significant. However, diethylnitrosamine and dimethylnitrosamine, which do not induce stomach cancer in rats, did not cause any decrease in pepsinogen content. Ethyl methanesulfonate, a direct-acting carcinogen used as a control, also did not decrease the pepsinogen content.
在非近交系雄性Wistar大鼠短期给予胃致癌物后,检测其胃幽门黏膜中胃蛋白酶原同工酶模式的变化。能在大鼠中诱发胃癌的N-甲基-N-硝基-N-亚硝基胍、N-乙基-N1-硝基-N-亚硝基胍和N-丙基-N-硝基-N-亚硝基胍,可降低通过聚丙烯酰胺凝胶电泳分离的胃蛋白酶原同工酶1(Pg 1)的含量。它们还降低了幽门黏膜中的胃蛋白酶原含量。在大鼠中诱发胃癌发生率较低的4-硝基喹啉-1-氧化物,很少降低Pg 1含量或幽门黏膜中的胃蛋白酶原含量,且这种降低的发生率无统计学意义。然而,在大鼠中不诱发胃癌的二乙基亚硝胺和二甲基亚硝胺,并未导致胃蛋白酶原含量有任何降低。用作对照的直接作用致癌物甲磺酸乙酯,也未降低胃蛋白酶原含量。