Retinyl succinate

In 1935 Hamano and Kawakami (1935) characterized retinol (1) as the P-naphthoate and anthraquinone P-carboxylate. Later Baxter and Robeson (1940) were able for the first time to obtain crystalline retinyl palmitate (113) and crystalline retinol (1) from liver oils. Crystalline retinyl acetate (9) and crystalline retinyl succinate were obtained at a later date (Baxter and Robeson, 1942). These very pure compounds made possible the accurate determination of a number of physical data. In 1946 Hanze et al. (1948) synthesized pure retinyl methyl ether (571) from crystalline retinol (1), and the total synthesis of this ether was reported at the same time by Milas et al. (1948). At this time also, syntheses of retinoids were carried out by Isler and associates and led to the first industrial synthesis of retinol derivatives (Isler et al., 1947 Isler, 1950 Heilbron and Weedon, 1958 Isler, 1979). 

Vitamin B2 phosphate sodium. See Riboflavin-5 -phosphate sodium Vitamin PP. See Niacinamide Vitamin A propionate. See Retinyl propionate Vitamin Q. See Ubiquinone Vitamin C sodium salt. See Sodium ascorbate Vitamin E succinate. See Tocopheryl succinate Vitamin Be tripalmitate. See Pyridoxine tripalmitate... 

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 12. A comparison of the proliferation (" H-thymidine incorporation) response of HCPC-1 cells following treatment with ascorbic acid and other agents (70 p-M, 6hr). The groups were as follows 1) untreated, 2) (i-carotene, 3) ascorbic acid, 4) a-tocopherol acid succinate, 5) retinyl palmitate, 6) canthaxanthin, 7) glutathione (ester), 8) glutathione (reduced), 9) glutathione (oxidized). Ascorbic acid treatment produced a profound reduction in proliferation at this dose and incubation period. 

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