کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2147014 | 1548385 | 2009 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Up-regulation of ROS by mitochondria-dependent bystander signaling contributes to genotoxicity of bystander effects
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کلمات کلیدی
Radiation-induced genomic instabilityDSBsDCFH-DAPDSDMSO - DMSODNA double-strand breaks - DNA دو رشته شکستهMitochondrial DNA - DNA میتوکندریاROS - ROSRadiation-induced bystander effect - اثر مواجهه ناشی از تابشBystander effects - اثرات متقابلionizing radiation - تابش یوننده یا پرتوهای یونیزانRoom temperature - دمای اتاقPopulation doublings - دو برابر جمعیتmtDNA - دیانای میتوکندریاییDimethyl sulfoxide - دیمتیل سولفواکسیدGenotoxicity - سمیت ژنتیکیRIBE - ماهیMitochondria - میتوکندریاsurvival fraction - کسری زنده ماندنReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Genomic instability can be observed in bystander cells. However, the underlying mechanism(s) is still relatively unclear. In a previous study, we found that irradiated cells released mitochondria-dependent intracellular factor(s) which could lead to bystander γ-H2AX induction. In this paper, we used normal (Ï+) and mtDNA-depleted (Ï0) human-hamster hybrid cells to investigate mitochondrial effects on the genotoxicity in bystander effect through medium transfer experiments. Through the detection of DNA double-strand breaks with γ-H2AX, we found that the fraction of γ-H2AX positive cells changed with time when irradiation conditioned cell medium (ICCM) were harvested. ICCM harvested from irradiated Ï+ cells at 10 min post-irradiation (Ï+ ICCM10 min) caused larger increases of bystander γ-H2AX induction comparing to Ï0 ICCM10 min, which only caused a slight increase of bystander γ-H2AX induction. The Ï+ ICCM10 min could also result in the up-regulation of ROS production (increased by 35% at 10 min), while there was no significant increase in cells treated with Ï0 ICCM10 min. We treated cells with dimethyl sulfoxide (DMSO), the scavenger of ROS, and quenched γ-H2AX induction by Ï+ ICCM. Furthermore, after the medium had been transferred and the cells were continuously cultured for 7 days, we found significantly increased CD59â gene loci mutation (increased by 45.9%) and delayed cell death in the progeny of Ï+ ICCM-treated bystander cells. In conclusion, the work presented here suggested that up-regulation of the mitochondria-dependent ROS might be very important in mediating genotoxicity of bystander effects.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 666, Issues 1â2, 18 June 2009, Pages 68-73
Journal: Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis - Volume 666, Issues 1â2, 18 June 2009, Pages 68-73
نویسندگان
Shaopeng Chen, Ye Zhao, Guoping Zhao, Wei Han, Lingzhi Bao, K.N. Yu, Lijun Wu,