Mitochondrial dysfunction resulting from loss of cytochrome c impairs radiation-induced bystander effect.
Cytochrome c is a pivotal protein that resides in mitochondria as component of mitochondria respiration and apoptosis initiator. Using murine cells lacking cytochrome c, we showed here that cytochrome c-deficient cells had attenuated reactive oxygen species/nitric oxide and micronuclei induction to radiation-induced bystander signals, indicating cytochrome c is essential for the bystander effect.
Yang
G
G
State Key Laboratory of Nuclear Physics and Technology, Peking University, Beijing 100871, People's Republic of China.
Wu
L
L
Chen
S
S
Zhu
L
L
Huang
P
P
Tong
L
L
Zhao
Y
Y
Zhao
G
G
Wang
J
J
Mei
T
T
Xu
A
A
Wang
Y
Y
D000818:Animals; D017209:Apoptosis; D024201:Bystander Effect / Q000528:radiation effects*; D018929:Cell Culture Techniques; D018920:Coculture Techniques; D045304:Cytochromes c / Q000378:metabolism*; D005720:Gamma Rays; D053078:Membrane Potential, Mitochondrial; D051379:Mice; D018345:Mice, Knockout; D015162:Micronucleus Tests; D008928:Mitochondria / Q000201:enzymology* / Q000473:pathology / Q000528:radiation effects*; D009569:Nitric Oxide / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D045304:Cytochromes c