Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells

Abstract

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.

Keywords

• Benzene toxicity
• Clusterin
• Hydroquinone
• Biomarker
• Apoptosis