Davies R J, Weidema W F, Sandle G I, Palmer L, Deschner E E, DeCosse J J
Cancer Res. 1987 Sep 1;47(17):4646-50.
Following 4 weeks of s.c. injections of 1,2-dimethylhydrazine, a carcinogen that produces colon cancer in CF1 mice, an increase in the unidirectional mucosal to serosal flux and net absorption of sodium was observed in the distal colon. This increase in sodium transport was amiloride sensitive. 1,2-Dimethylhydrazine treatment had no effect on sodium transport in the distal colon of DBA/2 mice, a strain which does not develop colonic malignant transformation. Although stimulation of sodium transport has been observed in cultured cell systems exposed to growth factors, similar changes in sodium transport have not previously been demonstrated in an intact epithelium at an early stage of carcinogenesis. The present study in mouse distal colon demonstrates that sodium transport is altered in 1,2-dimethylhydrazine-induced malignant transformation of the large bowel.
在对CF1小鼠皮下注射致癌物质1,2 - 二甲基肼4周后(该物质可使CF1小鼠患结肠癌),观察到其远端结肠黏膜向浆膜的单向通量和钠的净吸收增加。这种钠转运的增加对氨氯吡脒敏感。1,2 - 二甲基肼处理对DBA/2小鼠的远端结肠钠转运没有影响,DBA/2小鼠是一种不会发生结肠恶性转化的品系。尽管在暴露于生长因子的培养细胞系统中已观察到钠转运的刺激,但在致癌作用早期的完整上皮细胞中,此前尚未证实钠转运有类似变化。本项对小鼠远端结肠的研究表明,在1,2 - 二甲基肼诱导的大肠恶性转化过程中,钠转运发生了改变。