The aldehyde dehydrogenase (ALDH) superfamily contains NAD(P)<sup>+</sup>-dependent enzymes that metabolize a wide spectrum of aldehydes to their corresponding carboxylic acids. The human genome encodes nineteen ALDH isozymes. Missense mutations in ALDH genes are the molecular basis of several metabolic diseases, including Sjögren–Larsson syndrome (SLS), type II hyperprolinemia, γ-hydroxybutyric aciduria, pyridoxine-dependent seizures, De Barsy syndrome and spastic paraplegia, as well as alcohol-related diseases and late-onset Alzheimer’s disease. In addition to these identified clinical phenotypes, transgenic mouse models suggest crucial roles for ALDH isozymes in physiological processes, such as embryogenesis and development, and in protection against obesity and environmentally-induced oxidative damage.  ALDHs also appear to be involved in the biology of both normal stem cells and tumor-initiating stem cells. In tumors, ALDHs influence tumor growth and resistance to chemotherapy and radiation. In summary, these observations suggest that ALDHs may play pivotal roles in physiology and pathophysiology by metabolizing endogenous and exogenous aldehydes that are either toxic or essential for life.<br/>

Aldehyde dehydrogenases: From metabolic and alcohol-related diseases to cancer stem cells

2019 Fall National Meeting

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