The chemical properties of these two substances are strikingly similar.
Both compounds are irreversibly decomposed under biological conditions.
Alloxan has a half life of 1 minute (1) and dehydroascorbic acid has a half life of a few minutes (2). Alloxan is readily reduced to dialuric acid (3) with which it forms alloxantin (3). Dehydroascorbic acid is readily reduced to ascorbic acid (4) and also forms a similar intermediate compound (5). Alloxan (6) and dehydroascorbic acid (7) both form addition compounds with molecules containing the sulfhydryl group. Alloxan (8) and dehydroascorbic acid (9) both produce the Strecker reaction with amino acids and give the ordinary ketone reactions.
It would appear logical, therefore, to expect that there might be a relationship between alloxan and dehydroascorbic acid with regard to the production of diabetes. There is some evidence suggesting that dehydroascorbic acid may have diabetogenic properties. It is known that the dehydroascorbic acid level in the scorbutic animal is higher than normal,
the dehydroascorbic acid-ascorbic acid ratio being as much as 20 times the normal value (10). Correlated with this is the fact that scorbutic guinea pigs have a decreased glucose tolerance (11) and show degeneration of the islets of Langerhans (12). Furthermore, ascorbic acid is known to act synergistically with alloxan (13, 14) This is shown in the present work. It is also demonstrated that dehydroascorbic and dehydroisoascorbic acids produce diabetes in a manner similar to alloxan.
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Mhm... Its an old research but interesting nevertheless. My guess is that DHAA in such big doses blocks GLUT transporters so glucose can't enter the cells. Interestingly, they say:
Dehydroascorbic acid is more effective than ascorbic acid in acting synergistically with alloxan to produce diabetes.
Since alloxan is claimed not to be poisonous to beta cells in humans, like it is in other animals, its possible that effectiveness of alloxan in rats is due to AA synthesis (and so DHAA, especially as DHAA is not used by the rats but excreted by kidnies and that laboratory setup induces stress in animals which makes redox ratio DHAA/AA bigger). The reason is supposed to be species and dose dependent, altho there are no studies to support any such claim, particularly with longer low level exposures which might be typical for white bread consumers. In non patophysiological scenarios vitamin C exists in humans mostly as ascorbate acid.
This might mean that eating white flour products which contain small amounts of alloxan might be toxic to pancreas with Vitamin C megadoses. I personally removed white flour from the diet and since I take ~10g C daily, this might be a good thing to recommend to other megadosers.
Removing wheat from the diet should also be a good thing per se, given that number of diseases are caused by toxic wheat constituents like gluten and lectin.