Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1-7 |
| Number of pages | 8 |
| Journal | Mutation Research-Genetic Toxicology And Environmental Mutagenesis |
| Volume | 752 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - 15 Apr 2013 |
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Induction of sister chromatid exchange by acrylamide and glycidamide in human lymphocytes: Role of polymorphisms in detoxification and DNA-repair genes in the genotoxicity of glycidamide. / Pingarilho, Marta ; Oliveira, Nuno G.; Martins, Célia ; Gomes, Bruno Costa ; Fernandes, Ana Sofia ; Martins, Vanda; Labilloy, Anatalia; de Lima, João Pereira; Rueff, José; Gaspar, Jorge Francisco .
In: Mutation Research-Genetic Toxicology And Environmental Mutagenesis, Vol. 752, No. 1-2, 15.04.2013, p. 1-7.Research output: Contribution to journal › Article
TY - JOUR
T1 - Induction of sister chromatid exchange by acrylamide and glycidamide in human lymphocytes: Role of polymorphisms in detoxification and DNA-repair genes in the genotoxicity of glycidamide
AU - Pingarilho, Marta
AU - Oliveira, Nuno G.
AU - Martins, Célia
AU - Gomes, Bruno Costa
AU - Fernandes, Ana Sofia
AU - Martins, Vanda
AU - Labilloy, Anatalia
AU - de Lima, João Pereira
AU - Rueff, José
AU - Gaspar, Jorge Francisco
PY - 2013/4/15
Y1 - 2013/4/15
N2 - Acrylamide (AA) is a probable human carcinogen generated in carbohydrate-rich foodstuffs upon heating. Glycidamide (GA), formed via epoxidation, presumably mediated by cytochrome P450 2E1, is considered to be the active metabolite that plays a central role in the genotoxicity of AA. The aim of this work was to evaluate the cytogenetic damage induced by AA and GA in cultured human lymphocytes by use of the sister chromatid exchange (SCE) assay. Furthermore, this report addresses the role of individual genetic polymorphisms in key genes involved in detoxification and DNA-repair pathways (BER, NER, HRR and NHEJ) on the induction of SCE by GA. While AA induced the number of SCE/metaphase only slightly, especially for the highest concentration tested (2000 mu M) markedly induced SCEs in a concentration-dependent manner up to concentrations of 750 mu M, leading to an increase in SCEs of up to about 10-fold compared with controls. By combining DNA damage in GA-treated lymphocytes and data on polymorphisms, associations between the induction of SCEs with GSTP1 (Ile105Val) and GSTA2 (Glu210Ala) genotypes are suggested. (c) 2013 Elsevier B.V. All rights reserved.
AB - Acrylamide (AA) is a probable human carcinogen generated in carbohydrate-rich foodstuffs upon heating. Glycidamide (GA), formed via epoxidation, presumably mediated by cytochrome P450 2E1, is considered to be the active metabolite that plays a central role in the genotoxicity of AA. The aim of this work was to evaluate the cytogenetic damage induced by AA and GA in cultured human lymphocytes by use of the sister chromatid exchange (SCE) assay. Furthermore, this report addresses the role of individual genetic polymorphisms in key genes involved in detoxification and DNA-repair pathways (BER, NER, HRR and NHEJ) on the induction of SCE by GA. While AA induced the number of SCE/metaphase only slightly, especially for the highest concentration tested (2000 mu M) markedly induced SCEs in a concentration-dependent manner up to concentrations of 750 mu M, leading to an increase in SCEs of up to about 10-fold compared with controls. By combining DNA damage in GA-treated lymphocytes and data on polymorphisms, associations between the induction of SCEs with GSTP1 (Ile105Val) and GSTA2 (Glu210Ala) genotypes are suggested. (c) 2013 Elsevier B.V. All rights reserved.
KW - BREAST-CANCER SUSCEPTIBILITY
KW - CYTOGENETIC DAMAGE
KW - IN-VITRO
KW - RISK
KW - GLUTATHIONE S-TRANSFERASES
KW - DIETARY ACRYLAMIDE
KW - DNA-repair polymorphisms
KW - Sister chromatid exchange
KW - Detoxification
KW - Acrylamide
KW - Glycidamide
KW - HUMAN BLOOD
KW - CYTOCHROME-P450 2E1
KW - PORTUGUESE POPULATION
KW - COMMON VARIANTS
U2 - 10.1016/j.mrgentox.2012.12.013
DO - 10.1016/j.mrgentox.2012.12.013
M3 - Article
VL - 752
SP - 1
EP - 7
JO - Mutation Research-Genetic Toxicology And Environmental Mutagenesis
JF - Mutation Research-Genetic Toxicology And Environmental Mutagenesis
SN - 1383-5718
IS - 1-2
ER -