The Role of ROS in Hydroquinone-induced Inhibition of K562 Cell Erythroid Differentiation

The role of ROS in hydroquinone-induced inhibition of K562 cell erythroid differentiation was investigated. After K562 cells were treated with hydroquinone for 24 h, and hemin was later added to induce erythroid differentiation for 48 h, hydroquinone inhibited hemin-induced hemoglobin synthesis and...

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Bibliographic Details
Published in:Biomedical and environmental sciences 2014-03, Vol.27 (3), p.212-214
Main Authors: YU, Chun Hong, Suriguga, LI, Yang, LI, Yi Ran, TANG, Ke Ya, JIANG, Liang, YI, Zong Chun
Format: Article
Language:English
Subjects:
Acetylcysteine - pharmacology
Cell Differentiation - drug effects
Dose-Response Relationship, Drug
gamma-Globins - genetics
Hemin - pharmacology
Humans
Hydroquinones - pharmacology
K562 Cells - drug effects
K562细胞
L-半胱氨酸
Reactive Oxygen Species - metabolism
氢醌
氯化血红素
活性氧
浓度依赖性
红细胞分化
诱导
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Summary:The role of ROS in hydroquinone-induced inhibition of K562 cell erythroid differentiation was investigated. After K562 cells were treated with hydroquinone for 24 h, and hemin was later added to induce erythroid differentiation for 48 h, hydroquinone inhibited hemin-induced hemoglobin synthesis and mRNA expression of y-globin in K562 cells in a concentration-dependent manner. The 24-h exposure to hydroquinone also caused a concentration-dependent increase at an intracellular ROS level, while the presence of N- acetyI-L-cysteine prevented hydroquinone- induced ROS production in K562 cells. The presence of N-acetyI-L-cysteine also prevented hydroquinone inhibiting hemin-induced hemoglobin synthesis and mRNA expression of y-globin in K562 cells. These evidences indicated that ROS production played a role in hydroquinone-induced inhibition of erythroid differentiation.
ISSN:0895-3988
2214-0190
DOI:10.3967/bes2014.043