文献类型：期刊文献

英文题名：Multi-omics based strategy for toxicity analysis of acrylamide in Saccharomyces cerevisiae model

作者：Lin, Zhen[1];Luo, Ping[1];Huang, Dongmin[2];Wu, Yulian[1];Li, Fangping[1];Liu, Huazhong[1]

机构：[1]Guangdong Ocean Univ, Coll Chem & Environm Sci, Zhanjiang 524088, Peoples R China;[2]Shantou Univ, Dept Comp Sci, Shantou 515063, Peoples R China

年份：2021

卷号：349

外文期刊名：CHEMICO-BIOLOGICAL INTERACTIONS

收录：SCI-EXPANDED(收录号：WOS:000709947900003)、、Scopus(收录号：2-s2.0-85116148337)、WOS

基金：This work was supported by grants from the Natural Science Foundation of Guangdong Province (2019A1515011102) , China; the Project of Application-Based Talent Training Course from Guangdong Ocean University (570319017, 571119165) , China; the Postgraduate Educa-tion Innovation Program of Guangdong Ocean University (202146) , China.

语种：英文

外文关键词：Acrylamide; Transcriptome; Metabolome; Saccharomyces cerevisiae

外文摘要：Although the toxicity of acrylamide (ACR) has been extensively investigated in different experimental models, its perturbations to multiple nodes of the cellular signaling network have not been systematically associated. In this study, changes at different omics layers in ACR exposed Saccharomyces cerevisiae cells were monitored using a multi-omics strategy. The results of the analysis highlighted the impairment of oxidative-reductive balance, energy metabolism, lipid metabolism, nucleotide metabolism, and ribosome function in yeast cells. Response to acute ACR damage, glutathione synthesis was upregulated, the process of protein degradation was accelerated, and the autophagy flux was initiated. Meanwhile, yeast upregulates gene expression levels of enzymes in carbohydrate metabolism and speeds up the oxidation process of fatty acids to compensate for energy depletion. Importantly, the multi-omics strategy captures features that have rarely been addressed in previous studies on the toxicology of ACR, including blocked de novo nucleotide synthesis, decreased levels of metabolic enzyme cofactors thiamine and D-biotin, increased intracellular concentrations of neurotoxic N-methyl D-aspartic acid and L-glutamic acid, and release of death mediators ceramide. The ACR perturbation network constructed in this work and the discovery of new damage features provide a theoretical basis for subsequent point-to-point toxicological studies.