Allantoin as a Vitamin

Abstract

Inactivation of the gene ( Uox ) in primates, which is responsible for the synthesis of theenzyme urikase, has determined new ways of social and intellectual evolution of mammals [1, 2]. Almost simultaneously with this process, a mutation occurred, as a result of which primates lacked the capability of endogenous synthesis of ascorbate. These mutations sharply changed the systems of antioxidant defense by eliminating vitamin C and allantoin from the overall profile of intracellular nonenzymatic inactivation of reactive oxygen species. Water-soluble vitamins—active quenchers of intracellular free-radical processes—are characterized by a considerable similarity of biological effects, although the role of allantoin is more specific. This is also confirmed by the results of comparative analysis of thermodynamics of oxidation of ascorbic acid ( c 2 A ) and allantoin (Hall) by hydroxyl radicals, which was performed using quantum-chemical reagents [3, 4]. Earlier, it was shown experimentally and theoretically that allantoin is an effective antioxidant that is readily attacked by reactive oxygen species [3, 5]. It is also known that the reducing properties of ascorbic acid are the key factor that determines its function as a vitamin [4]. In aqueous medium, ascorbic acid dissociates according to the known scheme: When comparing hydroxylation of allantoin and dianion ascorbate, it is seen that the mechanisms of interaction of ascorbate and allantoin with the H radicals are different: allantoin 1 forms a fairly stable planar radical 2 [1], whereas ascorbate 3 is converted into stable dihydroascorbic acid 4 , inactivating two hydroxyl radicals [2]: