: To examine early changes in the cell membrane caused by treatment with 9.10-dimethyl-1.2-benzanthracene (DMBA), rat lingual epithelium in vitro was observed by means of electrophysiological, freeze-fracture and whole mount electron microscopic methods. Membrane potential showed a transient decrease at 6 h after the treatment but returned to almost the same level as that of the control group 1 day later. Membrane resistance decreased rapidly at 6 h after the treatment but increased at 12 h. Transient decrease of membrane resistance and membrane potential occurred prior to the decrease in coupling ratio at 6 h after treatment with DMBA. In freeze-fracture replicas, after 6 h of treatment with DMBA, the number of intramembranous particles (IMPs) was less than that of the control. This decrease was especially pronounced on the P-face. After 12 h treatment with DMBA, the number of IMPs increased by 20-40 % more than the control value. This increase was especially noticeable on the E-face, which was 70 % of the control value. At 3 days and thereafter, the number of IMPs decreased again and remained approximately the same as that of the control, though the Eface values remained larger than those of the control.Treatment with DMBA had a marked effect on the cytoskeletal organization.Treatment with DMBA caused morphologic changes as early as 6 h. These early changes might represent triggers for subsequent metabolic cellular abnormalities. The affected cells which were treated with DMBA appear to differ from normal cells through accelerated-abnormal cell membrane and cytoskeletal turnover.

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The distribution of fodrin in oral precancerous lesions and squamous cell carcinoma was examined by immunoperoxidase staining. In normal mucous epithelium and leukoplakia, fodrin was localized mainly along the plasma membrane of the granular, prickle and basal cells of the mucous epithelium. Diffused distribution was also observed in the cytoplasm of basal cells. In contrast, staining of fodrin was not clear in well-differentiated squamous cell carcinoma. It decreased markedly at the plasma membrane of the basal-like cells and slightly at the plasma membrane of prickle-like and glanular cells. However, diffused distribution of fodrin appeared in the cytoplasm of prickle-like and granular-like cells. In the cytoplasm of the basal-like cells, labeling of fodrin increased when compared with the basal cells of normal epithelium. In undifferentiated squamous cell carcinoma, fodrin labeling was absent at the plasma membrane of peripheral cells in the cancer nests.The present findings indicate that the pattern of fodrin staining was consistently absent at the peripheral edge of the proliferation area in the early stages of carcinoma and the cancer nest of undifferentiated squamous cell carcinoma, and that fodrin is related to cell differentiation and proliferation.

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