| Budget Amount *help |
¥34,580,000 (Direct Cost: ¥26,600,000、Indirect Cost: ¥7,980,000)
Fiscal Year 2020: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
Fiscal Year 2019: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
Fiscal Year 2018: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
Fiscal Year 2017: ¥6,760,000 (Direct Cost: ¥5,200,000、Indirect Cost: ¥1,560,000)
Fiscal Year 2016: ¥7,540,000 (Direct Cost: ¥5,800,000、Indirect Cost: ¥1,740,000)
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| Outline of Final Research Achievements |
The low level of ROS released by mitochondria in distress has been pointed out to be important for stress acclimation induction that is essential for organisms to overcome stresses. However, it remains unclear how mitochondria respond to stress and release small quantities of ROS. Here we demonstrated that N-acetyltyrosine functions as an intrinsic factor responsible for these tasks in stressed animals. All tested animals including insects and mice have N-acetyltyrosine in their blood, and its concentrations are elevated by heat stress. N-acetyltyrosine pretreatment causes perturbation of mitochondria, which causes a small increase in ROS production and leads to subsequent increase in their stress tolerance. In sum, we propose that N-acetyltyrosine is a vital endogenous molecule that could serve as a triggering factor for mitohormesis.
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