The permeability of normal, adenomatous, ulcerative colitic and malignant large bowel epithelial cell membranes to inulin.
We measured the permeability of normal, adenomatous, colitic and malignant large bowel epithelial cells by immersing fragments of large bowel mucosa in radiolabelled inulin and comparing autoradiograph grain density inside and outside cells after incubation. All the carcinomas studied showed extensive uptake of inulin within 5 min, while normal, adenomatous and colitic epithelial cells completely excluded inulin for 30 min. We found no difference in the proportion of epithelial cells incorporating uridine into RNA in carcinomatous and normal mucosa, and this suggests that the increased inulin permeability of carcinoma cell membranes was not due to leakage into non-viable cells. Experiments with cytochalasin B also showed that increased pinocytosis by carcinoma cells could not account for the difference. The relative impermeability of adenomatous and colitic cells suggests that increased permeability is not caused by increased proliferation. The consistent finding of increased permeability in the plasma membranes of carcinoma cells suggests that this may be more than an epiphenomenon of malignancy. It also suggests that measurement of cell permeability may have a role in distinguishing malignant from benign epithelial neoplasms.
D000236:Adenoma / Q000378:metabolism; D002463:Cell Membrane Permeability; D003093:Colitis, Ulcerative / Q000378:metabolism*; D003106:Colon / Q000378:metabolism*; D003110:Colonic Neoplasms / Q000378:metabolism*; D003571:Cytochalasin B / Q000494:pharmacology; D004848:Epithelium / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism; D007444:Inulin / Q000378:metabolism*; D010873:Pinocytosis / Q000187:drug effects; D012004:Rectal Neoplasms / Q000378:metabolism*
D003571:Cytochalasin B; D007444:Inulin