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Updated: Nov 4, 2025

Studying Chronic Exposure of Mice to Ultraviolet B Radiation
Published on: August 19, 2025
Metabolomics study of fibroblasts damaged by UVB and BaP
Xiaoyu Yang1, Jiateng Wang1, Hecong Wang1
1Beijing Key Laboratory of Plant Resources Research and Development, College of Chemistry and Meterials Engineering, Beijing Technology and Business University, Beijing, 100048, China.
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.
Insights
UVB and benzo(a)pyrene (BaP) damage skin cells by altering metabolism. This study reveals distinct metabolic changes in skin cells exposed to UVB, BaP, or both, highlighting key affected pathways like glycerophospholipid and glutathione metabolism.
Area of Science:
- Biochemistry
- Dermatology
- Toxicology
Background:
- Ultraviolet B (UVB) radiation and benzo(a)pyrene (BaP) are known carcinogens that can induce reactive oxygen species (ROS), apoptosis, and cancer.
- The specific metabolic alterations in skin following exposure to UVB, BaP, or their combination remain largely uncharacterized.
Purpose of the Study:
- To investigate and compare the metabolic profiles of human foreskin fibroblasts (HFF-1) after injury induced by UVB, BaP, or a combination of both.
- To elucidate the underlying metabolic mechanisms involved in skin damage caused by these agents.
Main Methods:
- Utilized ultra-performance liquid chromatography (UPLC) coupled with quadrupole time-of-flight mass spectrometry (qTOF-MS) to analyze metabolic changes.
- Examined metabolic profiles in HFF-1 cells exposed to UVB, BaP, and a combined UVB + BaP treatment.
Main Results:
- Significant alterations in metabolite levels were observed: 24 metabolites in the UVB group, 25 in the BaP group, and 33 in the combined UVB + BaP group.
- Key affected metabolites included glycerophosphocholine (PC), lactosylceramide (LacCer), guanidinosuccinic acid (GSA), glutathione (GSH), and lysophosphatidylcholine (LysoPC).
- Identified glycerophospholipid and glutathione metabolism as primary affected pathways.
Conclusions:
- UVB and BaP induce distinct metabolic perturbations in skin cells.
- Combined exposure to UVB and BaP results in a broader range of metabolic alterations compared to individual exposures.
- The findings provide critical insights into the molecular mechanisms of skin damage and carcinogenesis induced by UVB and BaP.
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