Abstract
Ethanol consumption and poor oral hygiene are risk factors for oral and oesophageal cancers. Although oral streptococci have been found to produce excessive acetaldehyde from ethanol, little is known about the mechanism by which this carcinogen is produced. By screening 52 strains of diverse oral streptococcal species, we identified Streptococcus gordonii V2016 that produced the most acetaldehyde from ethanol. We then constructed gene deletion mutants in this strain and analysed them for alcohol and acetaldehyde dehydrogenases by zymograms. The results showed that S. gordonii V2016 expressed three primary alcohol dehydrogenases, AdhA, AdhB and AdhE, which all oxidize ethanol to acetaldehyde, but their preferred substrates were 1-propanol, 1-butanol and ethanol, respectively. Two additional dehydrogenases, S-AdhA and TdhA, were identified with specificities to the secondary alcohol 2-propanol and threonine, respectively, but not to ethanol. S. gordonii V2016 did not show a detectable acetaldehyde dehydrogenase even though its adhE gene encodes a putative bifunctional acetaldehyde/alcohol dehydrogenase. Mutants with adhE deletion showed greater tolerance to ethanol in comparison with the wild-type and mutant with adhA or adhB deletion, indicating that AdhE is the major alcohol dehydrogenase in S. gordonii. Analysis of 19 additional strains of S. gordonii, S. mitis, S. oralis, S. salivarius and S. sanguinis showed expressions of up to three alcohol dehydrogenases, but none showed detectable acetaldehyde dehydrogenase, except one strain that showed a novel ALDH. Therefore, expression of multiple alcohol dehydrogenases but no functional acetaldehyde dehydrogenase may contribute to excessive production of acetaldehyde from ethanol by certain oral streptococci.
Highlights
Ethanol consumption has been recognized as a risk factor for several types of cancer, including the cancers of the head and neck, liver, colorectum and female breast (Bagnardi et al, 2001)
The second group included 38 clinical strains isolated from the saliva of 12 healthy volunteers. Their species were identified by 16S rRNA gene sequence to be Streptococcus gordonii, S. mitis, S. oralis, S. salivarius and S. sanguinis
V2016 was selected for further study of its enzymes involved in acetaldehyde production from ethanol
Summary
Ethanol consumption has been recognized as a risk factor for several types of cancer, including the cancers of the head and neck, liver, colorectum and female breast (Bagnardi et al, 2001). Excessive production of acetaldehyde from ethanol by oral bacteria (Homann, 2001; Kurkivuori et al, 2007) and from ethanol and/or sugar by oral fungi (Uittamo et al, 2009) may contribute to an increased risk of oral–oesophageal cancer. If a bacterium has both active ADH and ALDH, it can metabolize ethanol fully to the harmless acetic acid. If a bacterium has active ADH without ALDH, excessive acetaldehyde can be produced from ethanol. Acetaldehyde production by oral micro-organisms has been reported (Kurkivuori et al, 2007; Meurman & Uittamo, 2008), microbial enzymes involved have not been extensively studied
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