TY - JOUR
T1 - Radioprotective effects of ATP in human blood ex vivo.
AU - Swennen, E.L.
AU - Dagnelie, P.C.
AU - van den Beucken, A.M.
AU - Bast, A.
PY - 2008/1/1
Y1 - 2008/1/1
N2 - Damage to healthy tissue is a major limitation of radiotherapy treatment of cancer patients, leading to several side effects and complications. Radiation-induced release of pro-inflammatory cytokines is thought to be partially responsible for the radiation-associated complications. The aim of the present study was to investigate the protective effects of extracellular ATP on markers of oxidative stress, radiation-induced inflammation and DNA damage in irradiated blood ex vivo. ATP inhibited radiation-induced TNF-alpha release and increased IL-10 release. The inhibitory effect of ATP on TNF- alpha release was completely reversed by adenosine 5'-O-thiomonophosphate, indicating a P2Y(11) mediated effect. Furthermore, ATP attenuated radiation-induced DNA damage immediate, 3 and 6h after irradiation. Our study indicates that ATP administration alleviates radiation-toxicity to blood cells, mainly by inhibiting radiation-induced inflammation and DNA damage.
AB - Damage to healthy tissue is a major limitation of radiotherapy treatment of cancer patients, leading to several side effects and complications. Radiation-induced release of pro-inflammatory cytokines is thought to be partially responsible for the radiation-associated complications. The aim of the present study was to investigate the protective effects of extracellular ATP on markers of oxidative stress, radiation-induced inflammation and DNA damage in irradiated blood ex vivo. ATP inhibited radiation-induced TNF-alpha release and increased IL-10 release. The inhibitory effect of ATP on TNF- alpha release was completely reversed by adenosine 5'-O-thiomonophosphate, indicating a P2Y(11) mediated effect. Furthermore, ATP attenuated radiation-induced DNA damage immediate, 3 and 6h after irradiation. Our study indicates that ATP administration alleviates radiation-toxicity to blood cells, mainly by inhibiting radiation-induced inflammation and DNA damage.
U2 - 10.1016/j.bbrc.2007.12.125
DO - 10.1016/j.bbrc.2007.12.125
M3 - Article
C2 - 18164682
SN - 0006-291X
VL - 367
SP - 383
EP - 387
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -