Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells
Abstract Benzene is a crucial industrial hydrocarbon, posing significant health risks due to its toxic metabolites like hydroquinone (HQ). This study investigates the role of clusterin (CLU) in benzene toxicity by analyzing its protein and mRNA levels, as well as the expression of Bcl-2 and Bax, to...
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Nature Portfolio
2024-12-01
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| Series: | Scientific Reports |
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| Online Access: | https://doi.org/10.1038/s41598-024-82140-0 |
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| author | Peimao Li Qirui Gong Dianpeng Wang Zhimin Zhang Wen Zhang |
| author_facet | Peimao Li Qirui Gong Dianpeng Wang Zhimin Zhang Wen Zhang |
| author_sort | Peimao Li |
| collection | DOAJ |
| description | Abstract Benzene is a crucial industrial hydrocarbon, posing significant health risks due to its toxic metabolites like hydroquinone (HQ). This study investigates the role of clusterin (CLU) in benzene toxicity by analyzing its protein and mRNA levels, as well as the expression of Bcl-2 and Bax, to evaluate the feasibility of CLU as a biomarker for chronic benzene poisoning. HL-60 cells were induced to differentiate into neutrophil-like cells using 1% Dimethyl Sulfoxide (DMSO). Enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to analyze CLU protein and mRNA levels. ELISA was employed to detect sCLU protein content in cell culture supernatants, and western blot was used to assess Bcl-2 and Bax expression. The optimal time for 1% DMSO to induce HL-60 cells into neutrophil-like cells was 48 h. As HQ concentration increased, HL-60 cell viability decreased, CLU protein and sCLU protein levels in the supernatant decreased, CLU mRNA levels decreased, Bcl-2 protein expression decreased, and Bax expression increased. HQ exposure reduces CLU protein concentration and mRNA levels in neutrophil-like cells induced from HL-60 cells, indicating that CLU could be a potential biomarker for chronic benzene poisoning. |
| format | Article |
| id | doaj-art-e359517b778e4069b52700813c15f2fd |
| institution | OA Journals |
| issn | 2045-2322 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Nature Portfolio |
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| series | Scientific Reports |
| spelling | doaj-art-e359517b778e4069b52700813c15f2fd2025-08-20T02:31:00ZengNature PortfolioScientific Reports2045-23222024-12-0114111410.1038/s41598-024-82140-0Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cellsPeimao Li0Qirui Gong1Dianpeng Wang2Zhimin Zhang3Wen Zhang4Medical Laboratory, Shenzhen Prevention and Treatment Center for Occupational DiseasesMedical Laboratory College, Hebei North University in ChinaMedical Laboratory, Shenzhen Prevention and Treatment Center for Occupational DiseasesMedical Laboratory, Shenzhen Prevention and Treatment Center for Occupational DiseasesMedical Laboratory, Shenzhen Prevention and Treatment Center for Occupational DiseasesAbstract Benzene is a crucial industrial hydrocarbon, posing significant health risks due to its toxic metabolites like hydroquinone (HQ). This study investigates the role of clusterin (CLU) in benzene toxicity by analyzing its protein and mRNA levels, as well as the expression of Bcl-2 and Bax, to evaluate the feasibility of CLU as a biomarker for chronic benzene poisoning. HL-60 cells were induced to differentiate into neutrophil-like cells using 1% Dimethyl Sulfoxide (DMSO). Enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to analyze CLU protein and mRNA levels. ELISA was employed to detect sCLU protein content in cell culture supernatants, and western blot was used to assess Bcl-2 and Bax expression. The optimal time for 1% DMSO to induce HL-60 cells into neutrophil-like cells was 48 h. As HQ concentration increased, HL-60 cell viability decreased, CLU protein and sCLU protein levels in the supernatant decreased, CLU mRNA levels decreased, Bcl-2 protein expression decreased, and Bax expression increased. HQ exposure reduces CLU protein concentration and mRNA levels in neutrophil-like cells induced from HL-60 cells, indicating that CLU could be a potential biomarker for chronic benzene poisoning.https://doi.org/10.1038/s41598-024-82140-0Benzene toxicityClusterinHydroquinoneBiomarkerApoptosis |
| spellingShingle | Peimao Li Qirui Gong Dianpeng Wang Zhimin Zhang Wen Zhang Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells Scientific Reports Benzene toxicity Clusterin Hydroquinone Biomarker Apoptosis |
| title | Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells |
| title_full | Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells |
| title_fullStr | Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells |
| title_full_unstemmed | Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells |
| title_short | Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells |
| title_sort | clusterin mediates hydroquinone induced cytotoxic responses in hl 60 differentiated cells |
| topic | Benzene toxicity Clusterin Hydroquinone Biomarker Apoptosis |
| url | https://doi.org/10.1038/s41598-024-82140-0 |
| work_keys_str_mv | AT peimaoli clusterinmediateshydroquinoneinducedcytotoxicresponsesinhl60differentiatedcells AT qiruigong clusterinmediateshydroquinoneinducedcytotoxicresponsesinhl60differentiatedcells AT dianpengwang clusterinmediateshydroquinoneinducedcytotoxicresponsesinhl60differentiatedcells AT zhiminzhang clusterinmediateshydroquinoneinducedcytotoxicresponsesinhl60differentiatedcells AT wenzhang clusterinmediateshydroquinoneinducedcytotoxicresponsesinhl60differentiatedcells |