Linked Life Data

19393669

Source:http://linkedlifedata.com/resource/pubmed/id/19393669

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2009-6-1
pubmed:abstractText
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 gamma-H2AX induction. In this paper, we used normal (rho(+)) and mtDNA-depleted (rho(0)) 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 gamma-H2AX, we found that the fraction of gamma-H2AX positive cells changed with time when irradiation conditioned cell medium (ICCM) were harvested. ICCM harvested from irradiated rho(+) cells at 10 min post-irradiation (rho(+) ICCM(10 min)) caused larger increases of bystander gamma-H2AX induction comparing to rho(0) ICCM(10 min), which only caused a slight increase of bystander gamma-H2AX induction. The rho(+) ICCM(10 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 rho(0) ICCM(10 min). We treated cells with dimethyl sulfoxide (DMSO), the scavenger of ROS, and quenched gamma-H2AX induction by rho(+) ICCM. Furthermore, after the medium had been transferred and the cells were continuously cultured for 7 days, we found significantly increased CD59(-) gene loci mutation (increased by 45.9%) and delayed cell death in the progeny of rho(+) 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0027-5107
pubmed:author
pubmed:issnType
Print
pubmed:day
18
pubmed:volume
666
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
68-73
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Up-regulation of ROS by mitochondria-dependent bystander signaling contributes to genotoxicity of bystander effects.
pubmed:affiliation
Key Laboratory of Ion Beam Bioengineering, Institute of Plasma Physics, Chinese Academy of Sciences, Hefei 230031, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't