ROS 在对苯二酚诱导的 K562 细胞红系分化抑制中的作用。
The role of ROS in hydroquinone-induced inhibition of K562 cell erythroid differentiation.
机构信息
School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China.
出版信息
Biomed Environ Sci. 2014 Mar;27(3):212-4. doi: 10.3967/bes2014.043.
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.
研究了 ROS 在对苯二酚诱导的 K562 细胞红系分化抑制中的作用。用对苯二酚处理 K562 细胞 24 小时后，加入血红素诱导红系分化 48 小时，对苯二酚呈浓度依赖性抑制血红素诱导的 K562 细胞血红蛋白合成和 γ-珠蛋白 mRNA 表达。24 小时接触对苯二酚也导致细胞内 ROS 水平呈浓度依赖性增加，而 N-乙酰-L-半胱氨酸的存在可防止对苯二酚诱导 K562 细胞产生 ROS。N-乙酰-L-半胱氨酸的存在也可防止对苯二酚抑制血红素诱导的 K562 细胞血红蛋白合成和 γ-珠蛋白 mRNA 表达。这些证据表明，ROS 的产生在对苯二酚诱导的红系分化抑制中起作用。
Zotero 插件