@misc{oai:repo.qst.go.jp:00071255,
 author = {Wang, Zhenhua and Hong, Zhang and Bing, Wang and Tanaka, Kaoru and Zhou, Xin and Liu, Yang and Gan, Lu and Sun, Chao and Ｗａｎｇ Ｚｈｅｎｈｕａ and Ｈｏｎｇ Ｚｈａｎｇ and 王 冰 and 田中 薫 and Ｚｈｏｕ Ｘｉｎ and Ｌｉｕ Ｙａｎｇ and Ｇａｎ Ｌｕ and Ｓｕｎ Ｃｈａｏ},
 month = {Apr},
 note = {Radiation induced brain injury (RBI) is the most serious adverse reaction in cranial radiotherapy, which will cause the loss of neurons and cerebral capillary and finally result in the cognitive impairment. As the  power house  of cells, mitochondria play the essential role in keeping the stabilization of brain energy metabolism. However, the mitochondrial DNA (mtDNA) is a vulnerable target of irradiation, the injury of mtDNA might be the root of RBI. Here we used the mitochondria targeted antioxidant MitoQ to scavenge the intra-mitochondria reactive oxygen species (mtROS) and investigated the effects of mtROS in RBI induced by carbon ions. The long PCR results indicated that MitoQ significantly inhibited the mtDNA injury and downregulated the expression of PARP1 and ganma-H2AX. And the MitoQ pretreatment also improved the brain mitochondrial respiration function. The results indicated that the mtROS played key roles in RBI., 平成24年度HIMAC共同利用研究成果報告会},
 title = {Mitochondrial dysfunction induced by heavy-ion radiation in mouse brain: Does hypoxia play a role?},
 year = {2013}
}