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. 2017 Aug 29;7:9773. doi: 10.1038/s41598-017-09936-1

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic representation of the hypothesis proposed for the B[a]P-mediated metabolic flux redistribution. B[a]P exposure leads to the disturbance in the cellular redox state and hence to an increase in NADPH content of the cells by redirecting the metabolic flux towards the pentose phosphate pathway (PPP). It is indicated by the down-regulation of glycolytic proteins and an up-regulation of PPP proteins. The grey boxes represent the differentially regulated proteins identified by 2D BN/SDS-PAGE gel electrophoresis, whereas the pink boxes represent the metabolites identified by GC-MS analysis. Abbreviations: G6PD: glucose-6-phosphate dehydrogenase, GPI: glucose-6-phosphate isomerase isoform 1, ALD: fructose 1,6-bisphosphate, LDH: lactate dehydrogenase, FABP4: adipocyte fatty acid binding protein, 6GPL: 6-phosphogluconolactonase, NME: nucleoside diphosphate kinase, ATIC bifunctional purine biosynthesis protein, IDH1: cytosolic isocitrate dehydrogenase, ALDH1L1: 10-formyltetrahydrofolate dehydrogenase, THF: tetrahydrofolate, GSH: glutathione.