title: Catalytic removal of acetaldehyde in saliva by a Gluconobacter strain.
abstract: Acetaldehyde (AA) accumulates in the oral cavity after alcohol intake and is responsible for an increased risk of alcohol-related upper aerodigestive tract (UDAT) cancer among aldehyde dehydrogenase 2-inactive heterozygotes in particular. Thus, the removal of AA from the saliva to a level below its mutagenic concentration (50 μM) after drinking is a potentially straightforward method for reducing the risk of alcohol-related UDAT cancer. Although microbial cells with AA-decomposing activity could potentially serve as a useful agent for the catalytic removal of AA from the saliva without the supplemental addition of cofactors, these cells generally exhibit strong AA-producing activity from ethanol, which is present in excess (50mM) over AA (100 μM) in the saliva after drinking. In this study, we observed that Gluconobacter kondonii (GK) cells efficiently decomposed salivary AA (100-390 μM) without the supplemental addition of cofactors irrespective of the type of alcoholic beverages consumed, even in the presence of an excess of ethanol (63 mM). Hydrogen peroxide, which is carcinogenic in animal experiments, was not produced because of the AA removal. The GK cells incubated at 45 °C and pH 3.5 for 15 h were killed, but they retained 80% of their original AA-decomposing activity. The treated cells were used as nonviable microcapsules that harbor a membrane-bound AA-decomposing activity.
authors.affiliation: Department of Biomolecular Engineering, Graduate School of Engineering, Tohoku University, 6-6-11 Aza Aoba, Aramaki, Aoba-ku, Sendai, Miyagi 980-8579, Japan.
authors.forename: Haruhiko
authors.initials: H
authors.lastname: Yamaguchi
authors.forename: Miho
authors.initials: M
authors.lastname: Hosoya
authors.forename: Takefumi
authors.initials: T
authors.lastname: Shimoyama
authors.forename: Seiji
authors.initials: S
authors.lastname: Takahashi
authors.forename: Jian Feng
authors.initials: JF
authors.lastname: Zhang
authors.forename: Eri
authors.initials: E
authors.lastname: Tsutsumi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Yoshihide
authors.initials: Y
authors.lastname: Suwa
authors.forename: Toru
authors.initials: T
authors.lastname: Nakayama
mesh_terms: D000079:Acetaldehyde / Q000302:isolation & purification* / Q000378:metabolism*; D000428:Alcohol Drinking / Q000009:adverse effects* / Q000378:metabolism; D000434:Alcoholic Beverages / Q000009:adverse effects; D000444:Aldehyde Dehydrogenase / Q000172:deficiency / Q000235:genetics; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D002273:Carcinogens / Q000302:isolation & purification* / Q000378:metabolism; D002294:Carcinoma, Squamous Cell / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D000431:Ethanol / Q000009:adverse effects / Q000378:metabolism*; D020576:Gluconobacter / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D009055:Mouth / Q000378:metabolism / Q000473:pathology; D012463:Saliva / Q000737:chemistry / Q000378:metabolism*; D013696:Temperature
chemical_list: D002273:Carcinogens; D000431:Ethanol; C096127:ALDH2 protein, human; D000444:Aldehyde Dehydrogenase; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D000079:Acetaldehyde