74889-58-0Relevant articles and documents
Reaction of superoxide with ascorbic acid derivatives: Insight into the superoxide-mediated oxidation of dehydroascorbic acid
Frimer,Gilinsky-Sharon
, p. 2796 - 2801 (2007/10/02)
In order to gain greater insight into the mechanism of superoxide-mediated oxidation of ascorbic acid (1) in aprotic media, we reacted O2.- (generated from KO2/18-crown-6 in toluene) with vitamin C derivatives 13a and 14a and the corresponding mono- and dimethoxy analogs 13b and 13c, respectively. Dihydroxyfuranones 13a and 14a underwent oxidative cleavage with O2.- yielding, upon methyl iodide workup, the corresponding keto ester (15 or 17, respectively) and threonic acid analog (16 or 18, respectively). On the other hand, mono- and dimethoxy analogs 13b and 13c each react with superoxide to give a single isolable product, oxyester 16 and alkylidenefuranone 20, respectively. Finally, 13a reacts with tert-butoxide, again yielding 16 as the major product. The data are best resolved by suggesting that ascorbic acid analogs 13a and 14a (and presumably ascorbic acid as well) are oxidized by O2.- to the corresponding triketone 21 which reacts in turn by attack at the highly electrophilic central carbonyl C-2. Cyclization of the resulting 2-peroxy 1,3-diketone 22 into the C-1 carbonyl, followed by oxidative cleavage, saponification, and methylation, yields the observed products. By contrast, O2.- oxidation of 13b and tert-butoxide oxidation of 13a yield 3-peroxy-1,2-diketone 29 which cyclizes into the C-1 carbonyl ultimately yielding 16. Finally, 13c, which lacks enolic hydrogens, undergoes abstraction of the γ-hydrogen followed by the elimination of acetone, yielding 20. Similarly, 5,6-dihydropyrone 33 undergoes superoxide-mediated elimination yielding dienone 34. The data presented herein are consistent with the mechanism suggested by Sawyer et al. (J. Am. Chem. Soc. 1982, 104, 6273-6278) for the superoxide-mediated oxidation of dehydroascorbic acid (2) - with the modification that the position of initial O2.- attack is at the C-2 (rather than the C-3) carbonyl.
