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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Main Authors: Peimao Li, Qirui Gong, Dianpeng Wang, Zhimin Zhang, Wen Zhang
Format: Article
Language:English
Published: Nature Portfolio 2024-12-01
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.
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issn 2045-2322
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publishDate 2024-12-01
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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