Carbonyl Toxification Hypothesis of Biological Aging

Abstract

This chapter focuses on biochemical reactions known to be associated with the aging process, stresses the differences and similarities between free radical and glycation reactions, and proposes that toxification by di- and multicarbonyls is a ubiquitous and inevitable process that underlies biological aging. Carbonyl modification of biomolecules, a common consequence of free radical/Maillard reactions, is an important process of biological aging. The carbonyl toxification hypothesis of aging is also compatible with the finding that animals with a high metabolic rate have a shorter life span, probably because they also have an increased rate of carbonyl production. According to the free radical theory of aging, senescence and a variety of degenerative diseases associated with it are attributed primarily to the deleterious attack of oxygen free radicals on cellular constituents, including chromosomes, mitochondrial DNA, and connective tissues. Aminoguanidine is reported to be an effective drug in the prevention of diabetes-induced, glycation-related aging phenomena, for instance retinopathy or arterial wall protein cross-linking.