Fig. 1: Overview of the biological connections in AGE–alcohol–adduct formations. | Experimental & Molecular Medicine

Fig. 1: Overview of the biological connections in AGE–alcohol–adduct formations.

From: Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury

Fig. 1

Under conditions that increase lipid peroxidation, polyol pathway, and Maillard reaction, such as exposure to alcohol and/or high n-6 fat diets or high fructose drinks, different AGEs are produced. Ethanol and its reactive metabolites generated by CYP2E1 are also likely involved in the AGE synthesis pathways to produce the final acetaldehyde and AGE (AA-AGE) adducts. The formation of AA-AGE adducts can be observed after chronic alcohol exposure. These AA-AGE adducts exhibit similar properties (e.g., brown color and polymerization) as the AGE adducts cross-link with sugar molecules, and they are different from MAA adducts formed by AA and MDA interactions. However, treatment with an antioxidant can halt AA-AGE adduct formation, supporting the idea that AA-AGE adducts can be generated from a Schiff base product similar to AA adducts and AGEs.

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