| Project/Area Number |
22592093
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Pathobiological dentistry/Dental radiology
|
|---|
| Research Institution | Kagoshima University |
|---|
Principal Investigator |
MAJIMA Hideyuki 鹿児島大学, 大学院・医歯学総合研究科, 教授 (60165701)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
INDO Hiroko 鹿児島大学, 医歯学総合研究科, 助教 (00301391)
TOMITA Kazuo 鹿児島大学, 医歯学総合研究科, 助教 (60347094)
IWASHITA Youitirou 鹿児島大学, 医歯学総合研究科, 助教 (70168566)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
SUENAGA Shigeaki 鹿児島大学, 医学部・歯学部附属病院, 講師 (00136889)
|
|---|
| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
|---|
| Keywords | 頭頸部放射線治療 / 口腔粘膜障害 / アポトーシス / 内因性酸化ストレス抑制療法 / がん / 放射線治療 / ミトコンドリア / 活性酸素 |
|---|
| Research Abstract |
Human ells was transiently transfected with normal human MnSOD and MnSOD without a mitochondrial targeting signal (MTS). Mitochondrial reactive oxygen species (ROS), lipid peroxidation, and apoptosis were examined as a function of time following 18.8 Gy X-ray irradiation. The results showed that the level of mitochondrial ROS increased and reached a maximum level 2 h after X-ray irradiation. Authentic MnSOD, but not MnSOD lacking MTS, protected against mitochondrial ROS, lipid peroxidation, and apoptosis. In addition, the levels of mitochondrial ROS were consistently found to always correlate with the levels of authentic MnSOD in mitochondria. These results suggest that only when MnSOD is located in mitochondria is it efficient in protecting against cellular injuries by X-ray irradiation and that mitochondria are the critical sites of X-ray-induced cellular oxidative injuries.
|
