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Epigenetic effects of acrylamide exposure in mice

ABSTRACT: Acrylamide, a high-production-volume chemical and food contaminant in baked and fried carbohydrate-rich foods has been classiﬁed as a “Group 2A carcinogen” (probable human carcinogen) by the IARC. The carcinogenicity of acrylamide is attributed to its well-recognized genotoxicity; however, evidence suggests that acrylamide may also induce non-genotoxic alterations. In the present study female B6C3F1 mice were exposed to 0.70mM acrylamide in drinking water for 28 days and genotoxic and transcriptomic effects were investigated in the lung, a target organ for acrylamide carcinogenicity in mice, and the liver, a non-target organ. Acrylamide exposure resulted in a dose-dependent formation of N7-(2-carbamoyl-2-hydroxyethyl)guanine and N3-(2-carbamoyl-2-hydroxyethyl)adenine in lung and liver DNA at the similar levels. In contrast, whole genome gene expression profiles in the lungs and livers revealed the tissue-specific gene expression alterations. By using a SurePrint G3 Mouse Gene Expression v2 8x60K Microarray Kit (Agilent Technologies), we identified 123 and 363 genes that were found to be differentially expressed in the lungs and livers of acrylamide-treated mice; however, only 5 genes were in common between the organs. A detailed analysis of differentially expressed genes revealed that the major difference in the effect of acrylamide on the transcriptome in the lungs and livers was related to a different trend of gene expression changes. In the lungs, acrylamide exposure caused an inhibition of gene expression (54 up-regulated and 69 down-regulated genes), whereas the opposite effect, characterized by twice the number of up-regulated as compare to down-regulated genes (245 up-regulated and 118 down-regulated), was found in the livers of exposed mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE125851 | GEO | 2019/01/30

REPOSITORIES: GEO

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Project description:Many innovative techniques and scientific improvements are available to tackle societal concerns, like public health safety and confining the risk of cancerous exposure to chemicals, but have not been thoroughly tested and implicated yet. We investigated if microRNA and mRNA transcription profiles can be implemented in a short-term carcinogen classifier assay. Our study is additionally focusing on the drawbacks of present-day carcinogen screening strategies and also aims to contribute to a more ethical approach towards animal use and welfare within risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment. Since current in vitro and in silico assays are still not able to mimic the in vivo situation accurately we set out to develop an alternative short-term in vivo assay. Five genotoxic, seven non-genotoxic and five non-carcinogen exposure studies were used to investigate if murine hepatic microRNA and mNA profiles after 7-day exposure are suitable tools to classify carcinogens. Classification analyses showed that a small transcript set, consisting of both microRNA and mRNA, is able to classify the genotoxic, non-genotoxic and non-carcinogens tested with 100% accuracy. The results indicate that microRNAs have the potential to be used as transcriptional classifiers and that a short-term transcriptional classifier assay in mice can be a powerful tool in carcinogenicity risk assessment. [mRNA profling] 96 hepatic samples in total, 8 control untreated samples, replicates per treated group n=4-6

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Epigenetic effects of acrylamide exposure in mice

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