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Acetaldehyde production by non‐pathogenic Neisseria in human oral microflora: Implications for carcinogenesis in upper aerodigestive tract
Author(s) -
Muto Manabu,
Hitomi Yoshiaki,
Ohtsu Atsushi,
Shimada Hiroyuki,
Kashiwase Yukiko,
Sasaki Hiroki,
Yoshida Sigeaki,
Esumi Hiroyasu
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20001101)88:3<342::aid-ijc4>3.0.co;2-i
Subject(s) - acetaldehyde , carcinogen , alcohol dehydrogenase , microbiology and biotechnology , biology , ethanol , carcinogenesis , alcohol , ingestion , metabolite , bacteria , cancer , biochemistry , genetics
Many epidemiological studies have identified chronic alcohol consumption as a significant risk factor for cancer of the upper aerodigestive tract (UAT) in human. Although acetaldehyde, the first metabolite from ethanol by alcohol dehydrogenase (ADH), is regarded as a carcinogen, how systemic production of acetaldehyde particularly affects the UAT remains unclear. In our study, we searched for the regional source of acetaldehyde in UAT, especially the involvement of bacteria in the human normal oral microflora. Here we demonstrate that, among the bacterial species identified from the human oral cavity, genus Neisseria had extremely high ADH activity and produced significant amounts of acetaldehyde when cultured with medium containing ethanol in vitro. The ability to produce acetaldehyde was more than 100‐fold higher than that produced by any other genera we studied. Furthermore, alcohol ingestion influences the bacterial composition of the oral microflora, resulting in an increased proportion of Neisseria . Although Neisseria present in normal oral microflora is generally non‐pathogenic, these findings suggest that this microbe can be a regional source of carcinogenic acetaldehyde and thus potentially play an important role in alcohol‐related carcinogenesis in human UAT. Int. J. Cancer 88:342–350, 2000. © 2000 Wiley‐Liss, Inc.