Metabolomics study of fibroblasts damaged by UVB and BaP

Xiaoyu Yang,Hecong Wang,Jiateng Wang,Congfen He,Lei Liu,Xueying Li

doi:10.1038/s41598-021-90186-7

Xiaoyu Yang, Hecong Wang + Show 4 more

Open Access

https://doi.org/10.1038/s41598-021-90186-7

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Journal: Scientific Reports	Publication Date: May 27, 2021
Citations: 5	License type: open-access

Affiliation: Beijing Technology and Business University

Abstract

We have recently shown that both UVB and BaP can induce the production of ROS, apoptosis and even cancer. However, the differences in the metabolic profiles of skin damaged by UVB, BaP or UVB combined with BaP have not been studied. Therefore, we examined the metabolic changes in the human foreskin fibroblast injured by UVB or BaP or the combination of the two, using ultra performance liquid chromatography (UPLC) coupled with quadrupole time-of-flight mass spectrometry (qTOF-MS). 24 metabolites were altered in the UVB damage group, 25 in the BaP damage group, and 33 in the UVB combined with BaP group. These alterations indicated that the metabolic mechanisms of HFF-1 cells treated with UVB or BaP are related to multiple main metabolites including glycerophosphocholine (PC), lactosylceramide (LacCer), guanidinosuccinic acid (GSA), glutathione(GSH), and lysophosphatidylcholine (LysoPC) and the main mechanisms involved glycerophospholipid and glutathione metabolism. Thus, our report provided useful insight into the underlying mechanisms of UVB and BaP damage to skin cells.

Highlights

We have recently shown that both Ultraviolet B (UVB) and BaP can induce the production of ROS, apoptosis and even cancer
Significant decreases in triglycerides and total free fatty acids have been found in the epidermis after acute and chronic exposure of human skin to UV r adiation[7], and these changes in free fatty acids in the skin after UV treatment have been associated with fatty acid synthesis[8]
UVB irradiation and BaP both lead to increased oxidation in the human skin cells.the cytotoxicity of BaP against HFF-1 cells was determined by measuring the level of intracellular ROS generation

Summary

Introduction

We have recently shown that both UVB and BaP can induce the production of ROS, apoptosis and even cancer. metabolites were altered in the UVB damage group, in the BaP damage group, and 33 in the UVB combined with BaP group These alterations indicated that the metabolic mechanisms of HFF-1 cells treated with UVB or BaP are related to multiple main metabolites including glycerophosphocholine (PC), lactosylceramide (LacCer), guanidinosuccinic acid (GSA), glutathione(GSH), and lysophosphatidylcholine (LysoPC) and the main mechanisms involved glycerophospholipid and glutathione metabolism. Abbreviations ASA Argininosuccinate BaP Benzo[a]pyrene CoA Coenzyme A DCFH-DA Oxidation-sensitive dye 2′,7′-dichlorofluorescin diacetate DMEM High glucose Dulbecco’s Modified Eagle Medium DPE Diesel particulate extract EGF Epidermal growth factor EGFR Epidermal growth factor recepter GM3 NeuAcα2 → 3Galβ1 → 4Glcβ1 → 1Cer. GSA Guanidinosuccinic acid GSH Glutathione GSSG Glutathione disulphide HaCaT Human Keratinocytes Cell HFF-1 Human fibroblasts cells HMDB Human Metabolome Database IL Interleukin LacCer Lactosylceramide LysoPC Lysophosphatidylcholine LysoPE Lysophosphatidylethanolamine PA Phosphatidic acid PAHs Polycyclic aromatic hydrocarbons PBS Phosphate buffered saline PC Glycerophosphocholine PE Glycerophosphoethanolamine PG Phosphatidylglycerol PS Phosphatidylserine SM Sphingomyelin TG Monodocosahexaenoic acid triglyceride TNFα Serum tumor necrosis factor. Fatty acids played an important role in controlling inflammation in UVB-irradiated mouse skin tests, especially saturated fatty a cids[8]

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