Oral Intake of Anti-Hangover Substance Increases Metabolizing Capacity of Aldehyde Dehydrogenase 2 in Rat Model: New Therapeutic Potentials for Chronic Itch ?
Monday, March 7, 2016
South Exhibit Hall H (Convention Center)
Bossng Kang, Chae-Young Bang, Se-Young Choung, Kyungwoo Choi
Rationale:  Aldehyde dehydrogenase 2 (ALDH 2) metabolizes acetaldehyde, the major cause of alcohol hangover symptoms. It also detoxifies endogenous cytotoxic aldehydes, such as 4-hydroxynonenal. Oxidative stress promotes lipid peroxidation of cellular membrane, leading to the accumulation of reactive aldehydes that contribute to itch signaling via mast cell degranulation and the activation of TRPA1 on sensory neuron. A variety of anti-hangover products are commercially available, however, almost none of them has been proven to show enhanced metabolizing capacity of ALDH 2 in a live subject. We aimed to test a specific product of interest. Methods:  An anti-hangover product (KISLip, Pico Entech, Korea) was examined by in vitro & in vivo experiments to measure the amount of NADH formation which is generated through catalytic conversion of acetaldehyde. Powder sample was used as the experimental substance. In-vivo examination tested the ethanol and acetaldehyde level in blood of rats with oral infusion of substance before or after ethanol intake. Results:  The activities of alcohol dehydrogenase & aldehyde dehydrogenase within the anti-hangover substance were 1.84 unit/g and 0.28 unit/g, respectively. The oxidation capacities in experimental rats were dose-dependently increased after substance gavages. Particularly, the cases with oral intake of substance 220 mg/kg after 1hr of ethanol intake have shown more meaningful and obvious decreases in acetaldehyde level in blood. Conclusions:  Oral intake of anti-hangover substance has significantly enhanced acetaldehyde-metabolizing capacity in rat model, potentially suggesting increased ALDH 2 capacity within circulation and detoxifying ability of 4-hydroxynonenal.