We have previously shown that acetaldehyde is produced by (Collings et al., in vitro C. albicans 1991) and more recent studies have suggested that oral colonisation with and other C. albicans yeast can contribute to the presence of acetaldehyde in saliva (Nieminen et al., 2009, et al., 2013, Marttila et al., 2013a, Marttila et al., 2013b). Intriguingly, Marttila et al (2013a) reported that under low oxygen tension there was no correlation between in vitro acealdehyde concentration and RNA expression, but rather with expression of RNA ADH1 ADH6 (encoding an acetaldehyde utilising enzyme). However, as noted by these authors, Adh1p levels do not correlate closely with mRNA levels (Bertram et al., 1996), possibly due to ADH1 or post-transcriptional control. Indeed, Adh1p is upregulated in biofilm formation (Martinez-Gomariz et al., 2009) and oral biofilms can contain (Zijnge et al., 2010). C. albicans We conclude that of two members of the gene family (ADH1 and were ADH ADH2) expressed under growth conditions replicating both replete and minimal nutritional conditions. Furthermore expression of Adh1p, but not Adh2p, conferred ethanol utilisation C. albicans activity when heterologously expressed in Although regulation of other enzymes S. cerevisiae. involved in acetaldehyde metabolism, such as Adh6p, may be involved in the accumulation of acetaldehyde in cultures or we suggest that the high expression of Adh1p by in vivo, C. albicans, and its ethanol utilising activity, can contribute to the generation of the carcinogen acetaldehyde in the saliva of colonised individuals. ACKNOWLEDGEMENTS MM Bakri was supported by a postgraduate scholarship from the University of Malaya and this work was also supported by the New Zealand Dental Association Research Foundation. We are grateful for the free availability of the and genome databases Candida Saccharomyces (CGD; http://www.candidagenome.org/ and SGD; http://www.yeastgenome.org/).
We have previously shown that acetaldehyde is produced in vitro by C. albicans (Collings et al., 1991) and more recent studies have suggested that oral colonisation with C. albicans and other yeast can contribute to the presence of acetaldehyde in saliva (Nieminen et al., 2009, et al., 2013, Marttila et al., 2013a, Marttila et al., 2013b). Intriguingly, Marttila et al (2013a) reported that under low oxygen tension in vitro there was no correlation between acealdehyde concentration and ADH1 RNA expression, but rather with expression of ADH6 RNA (encoding an acetaldehyde utilising enzyme). However, as noted by these authors, Adh1p levels do not correlate closely with ADH1 mRNA levels (Bertram et al., 1996), possibly due to or post-transcriptional control. Indeed, Adh1p is upregulated in biofilm formation (Martinez-Gomariz et al., 2009) and oral biofilms can contain C. albicans (Zijnge et al., 2010). We conclude that of two members of the ADH gene family (ADH1 and ADH2) were expressed under growth conditions replicating both replete and minimal nutritional conditions. Furthermore expression of C. albicans Adh1p, but not Adh2p, conferred ethanol utilisation activity when heterologously expressed in S. cerevisiae. Although regulation of other enzymes involved in acetaldehyde metabolism, such as Adh6p, may be involved in the accumulation of acetaldehyde in cultures or in vivo, we suggest that the high expression of Adh1p by C. albicans, and its ethanol utilising activity, can contribute to the generation of the carcinogen acetaldehyde in the saliva of colonised individuals. ACKNOWLEDGEMENTS MM Bakri was supported by a postgraduate scholarship from the University of Malaya and this work was also supported by the New Zealand Dental Association Research Foundation. We are grateful for the free availability of the Candida and Saccharomyces genome databases (CGD; http://www.candidagenome.org/ and SGD; http://www.yeastgenome.org/).
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