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Mutagenesis Advance Access originally published online on April 11, 2008
Mutagenesis 2008 23(4):309-315; doi:10.1093/mutage/gen016
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© The Author 2008. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

Acrylamide-induced molecular mutation spectra at HPRT locus in human promyelocytic leukaemia HL-60 and NB4 cell lines

Lin Ao, Sheng-Xue Liu, Meng-Su Yang1, Chi-Chun Fong1, Hui An and Jia Cao*

Department of Hygienic Toxicology, Preventive Medical College, Third Military Medical University, Chongqing 400038, People's Republic of China 1Department of Biology and Chemistry, City University of Hong Kong, Kowloon 83, Hong Kong, People's Republic of China

Acrylamide (AA) is a compound widely used in many industries around the world. The recent finding that it is formed naturally in foods by heating raises human health concerns. AA is a proven carcinogen in animals and a probable carcinogen in humans, while its mutagenicity detected using in vitro mammalian gene mutation assays is still inconsistent in different cell systems. In the present study, we investigated the mutagenicity of AA in human promyelocytic leukaemia cells, HL-60 and NB4 cells, by examining the mutations at the hypoxanthine–guanine phosphoribosyltransferase (HPRT) gene locus. In a 6-h treatment without the exogenous activation, AA exerted a weak mutagenic effect at the highest concentration used in the study (700 mg/l) in HL-60 cells (P < 0.01) as well as in NB4 cells (P < 0.05). Molecular analysis of AA-induced mutants revealed a different mutation spectrum, when compared to that of spontaneous mutants. The most frequent spontaneous mutations were point mutations, whereas AA-induced mutations were mainly single exon deletions besides point mutations, and an increase in the proportion of partial deletion was associated with the increase of AA treatment. There was no obvious difference in the mutation spectra observed between the HL-60 and NB4 cell lines. These results showed that AA has a weak mutagenic effect at HPRT gene locus in human promyelocytic leukaemia HL-60 and NB4 cell lines and those molecular mutation spectra (single exon deletions and point mutations) may be related to some specific and precise mechanism.

* To whom correspondence should be addressed. Tel: +86 023 68752271; Fax: +86 023 68752277; Email: caojia{at}mail.tmmu.com.cn

Received on January 22, 2007; revised on February 26, 2008; accepted on February 27, 2008.


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