The role of ROS in hydroquinone-induced inhibition of K562 cell erythroid differentiation.

Author: Chun Hong YU ¹ ; Suriguga ¹ ; Yang LI ¹ ; Yi Ran LI ¹ ; Ke Ya TANG ¹ ; Liang JIANG ¹ ; Zong Chun YI ¹
Author Information

1. School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China.
Publication Type:Journal Article
MeSH: Acetylcysteine; pharmacology; Cell Differentiation; drug effects; Dose-Response Relationship, Drug; Hemin; pharmacology; Humans; Hydroquinones; pharmacology; K562 Cells; drug effects; Reactive Oxygen Species; metabolism; gamma-Globins; genetics
From: Biomedical and Environmental Sciences 2014;27(3):212-214
CountryChina
Language:English
Abstract: 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 γ-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- acetyl-L-cysteine prevented hydroquinone- induced ROS production in K562 cells. The presence of N-acetyl-L-cysteine also prevented hydroquinone inhibiting hemin-induced hemoglobin synthesis and mRNA expression of γ-globin in K562 cells. These evidences indicated that ROS production played a role in hydroquinone-induced inhibition of erythroid differentiation.