Protooncogene and Oncogene Products

To substantiate the results observed in the above assays, immunohistochemical studies were carried out for c-neu/erb-B2, EGFR, c-jun, c-fos, and Bcl-2. After treatment with ascorbic acid there was a reduced expression of Bcl-2, EGFR, and c-jun. C-fos expression was increased. These findings demonstrated that ascorbic 

FIGURE 8. Nucleosome formation in a human oral carcinoma cell line (SCC-25) was observed following treatment with ascorbic acid (20 xM, 3hr) (A), in comparison to untreated tumor cells (B). 

FIGURE 9. A comparison of the apoptotic response produced by ascorbic acid treatment compared to other antioxidant treatments. SCC-25 cells were stained for nucleosome formation as shown in Fig. 8. The relative number of apoptotic cells per 100 cells was counted. The treatment groups were 1) canthaxanthin, 2) p-carotene, 3) retinyl palmitate, 4) a-tocopherol acid succinate, 5) ascorbic acid, 6) glutathione (reduced), and 7) glutathione (oxidized). The treatment doses were 20, 10, and 1.25 fxM. 

FIGURE 10. The total mercaptan concentration was ascertained following various treatments. The treatment with ascorbic acid (70 jxM, 6 hr) produced a significant reduction of mercaptans in a hamster oral carcinoma cell line (HCPC-1). The treatments were as follows 1) untreated, 2) p-carotene, 3) a-tocopherol acid succinate, 4) canthaxanthin, 5) reduced glutathione, 6) retinyl palmitate, 7) ascorbic acid. 

FIGURE 11. Changes in the intracellular glutathione following treatment with the chemopreventive agents. The treatments were identical to those in Fig. 10. Ascorbic acid treatment reduced the level of glutathione in the tumor cell line (HCPC-1). 

---