Project/Area Number |
22590873
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
|
Research Institution | Nippon Medical School |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
OHSAWA Ikuro 日本医科大学, 老人病研究所, 教授 (30343586)
FUKUDA Yuh 日本医科大学, 大学院・医学研究科, 教授 (60097037)
TERASAKI Mika 日本医科大学, 医学部, 助教 (50372785)
|
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: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 酸化ストレス / 水素還元力 / 呼吸器疾患 / 水素抗酸化作用 / 放射線肺障害 / アポトーシス / ハイドロキシラジカル / クララ細胞 / ゲフィチニブ / ナフタレン / 抗酸化作用 |
Research Abstract |
Various lung injuries such as irradiation or anticancer drug induced injuries are reportedly initiated and sustained by oxidative stress (reactive oxygen species:ROS), especially hydroxyl radicals (-OH), which are the primary cause of the damage. As yet,no ideal ROS scavenge therapy has been established. Because H2 was recently reported as an efficient antioxidant that diffuses rapidly across cell membranes, selectively reduces -OH, and suppresses oxidative stress-induced injury with no known toxicity, we studied the possibility that H2 could protect against irradiation or anticancer drug induced lung damage. We show here that H2 scavenged -OH and protected against apoptotic damage related to oxidative stress induced by irradiation and anticancer drug in lung epithelial cells and in lungs of mice. H2 treatment will thus be valuable for protection against oxidative stress induced various lung diseases.
|