Abstract
Heterocyclic amines (HCAs) are a set of food contaminants that may exert a cytotoxic effect on human peripheral blood mononuclear cells (PBMC). However, the genetic mechanism underlying the cytotoxicity of HCAs on PBMC has not been investigated. In the study, bioinformatic analysis on gene dataset GSE19078 was performed. The results of weighted correlation network analysis and linear models for microarray and RNA-seq data analysis showed that four gene modules were relevant to 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) exposure while one gene module was correlated with 2-amino-3-methyl-3H-imidazo[4,5f]quinoline (IQ) exposure. Gene functional analysis showed that the five modules were annotated mainly with mRNA transcriptional regulation, mitochondrial function, RNA catabolic process, protein targeting, and immune function. Five genes, MIER1, NDUFA4, MLL3, CD53 and CSF3 were recognized as the feature genes for each hub gene network of the corresponding gene module, and the expression of feature genes was observed with a significant difference between the PhIP/IQ samples and the other samples. Our results provide novel genes and promising mechanisms for exploration on the genetic mechanism of HCAs on PBMC.
Highlights
Heterocyclic amines (HCAs) are potential mutagens ubiquitously existing in cooked protein-rich food such as fried fish and roasted meat [1]
These results show a good quality of the data and a similarity among the expression profile within the IQ dosed group or the PhIP group
In the present study, we investigated the genetic mechanism underlying the cytotoxic effect of HCAs on peripheral blood mononuclear cells (PBMC) by analyzing the Gene Expression Omnibus (GEO) database GSE19078 through bioinformatic methods
Summary
Heterocyclic amines (HCAs) are potential mutagens ubiquitously existing in cooked protein-rich food such as fried fish and roasted meat [1]. Hiding behind the tempting flavor and rich nutrients of grilled food, HCAs are inevitably consumed by and absorbed into human bodies and exert toxicological effects [2]. As carcinogenic xenobiotics consumed with diet and absorbed by the digestive tract, HCAs have been found to exert their carcinogenic effect in the colon [4]. The potential mechanism underlying the carcinogenicity of HCAs includes oxidative stress, DNA damage, endocrine disruption, etc. Only a few studies have focused on the immunotoxicology of HCAs and their cytotoxic effect on immune cells, and little information is known about the underlying mechanism of cyotoxicology of HCAs on immune cells. A recent study investigated the genotoxicity of HCAs on isolated human peripheral blood mononuclear cells (PBMC), suggesting a DNA damage effect of HCAs on PBMC [9]. The other mechanisms, especially the genetic mechanism, behind the cytotoxic effect of HCAs on PBMC has not been elucidated
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