Oral intake of anti-hangover substance increases aldehyde dehydrogenase activity: New preventive and therapeutic potentials for oxidative neuronal injury?

Abstract

Objectives: Acetaldehyde is a major cause of alcohol hangover symptoms, which is primarily metabolized by mitochondrial aldehyde dehydrogenase. This enzyme plays a crucial role in maintaining normal mitochondrial function to protect against neurotoxicity by detoxification of other cytotoxic aldehydes. Although a variety of anti-hangover products are commercially available, almost none of them has been proven to show enhanced activity of aldehyde dehydrogenase in a live subject. We aimed to investigate a specific product of interest. Methods: The enzyme activities of the anti-hangover candy were examined by in vitro & in vivo experiments to measure the amount of NADH formation which is generated through catalytic conversion of alcohol and acetaldehyde. Powder sample of a commercial anti-hangover product (KISLip®, Pico Entech, South Korea) was used as the experimental substance. In-vivo examination tested the ethanol and acetaldehyde concentration in blood of rats with oral infusion of experimental substance before or after ethanol intake. Results: In vitro measurements of the activities of alcohol dehydrogenase & aldehyde dehydrogenase within the anti-hangover substance were 1.84 unit/g and 0.28 unit/g, respectively. The enzyme activities in experimental rats were significantly increased after substance gavages (Fig. 1). Conclusions: Oral intake of anti-hangover substance has significantly enhanced enzyme activities of alcohol metabolism in rat model, particularly aldehyde dehydrogenase activity within circulation. Using this substance, further research on diseased animal model is recommended to conduct.