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Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells
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Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells
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Journal Article
Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells
2024
Overview
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 692/53
/ bcl-2-Associated X Protein - genetics
/ bcl-2-Associated X Protein - metabolism
/ Benzene
/ Cell Differentiation - drug effects
/ Cell Survival - drug effects
/ Enzyme-linked immunosorbent assay
/ Humanities and Social Sciences
/ Humans
/ mRNA
/ Proteins
/ Proto-Oncogene Proteins c-bcl-2 - genetics
/ Proto-Oncogene Proteins c-bcl-2 - metabolism
/ Science
