Effect of Carnosine and Related Compounds on Glucose Oxidation and Protein Glycation In Vitro

The effects of carnosine and related compounds (CRC) including anserine, homocarnosine, histidine, and ${\beta}$-alanine, found in most mammalian tissues, were investigated on in vitro glucose oxidation and glycation of human serum albumin (HSA). Carnosin and anserine were more reactive with D-glucose than with L-lysine. In the presence of $10\;{\mu}M$ Cu (II), although carnosine and anserine at low concentrations effectively inhibited formation of ${\alpha}$-ketoaldehyde from D-glucose, they increased generation of $H_2O_2$ in a dose-dependent manner. Carnosine, homocarnosine, anserine, and histidine effectively inhibited hydroxylation of salicylate and deoxyribose degradation in the presence of glucose and $10\;{\mu}M$ Cu (II). In the presence of 25 mM D-glucose, copper and ascorbic acid stimulated carbonyl formation from HSA. Except for ${\beta}$-alanine, CRC effectively inhibited the copper-catalyzed carbonyl formation from HSA. The addition of 25 mM D-glucose and/or $10\;{\mu}M$ Cu (II) to low density lipoprotein (LDL) increased formation of conjugated dienes. CRC effectively inhibited the glucose and/or copper-catalyzed LDL oxidation. CRC also inhibited glycation of HSA as determined by hydroxymethyl furfural and lysine with free ${\varepsilon}$-amino group. These results suggest that CRC may play an important role in protecting against diabetic complications by reacting with sugars, chelating copper, and scavenging free radicals.