| Budget Amount *help |
¥3,750,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥150,000)
Fiscal Year 2007: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2006: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Research Abstract |
Up to now, carbon monoxide (CO) has been considered to be a poisoning material. It was assumed the toxicity was for CO to attach strongly to the hemoglobin in the red blood cells, and to cause hypoxia. However, it was found that there was CO in a human expiration, and CO was generated when hemoglobin were decomposed. In 1968 the enzyme hem-oxygenase (HO), which resolves hemoglobin, was discovered
On the other hand, CO has a vasodilatory effect. From similarity with NO, it is assumed that CO has an action as intracellular transmitter. Afterwards, the inhibition of CO on apoptosis and an anti-inflammatory effects of CO were clarified, and it was shown that CO had both the cell toxicity and the cell protection effect.
HO-1 is inducible subtype of HO. It was reported that HO-1 is induced due to oxidative stress, ischemia/reperfusion, inflammation, and so on. It is shown that HO-1 is found in arteriosclerosis part in the vessel recently.
To study the participation of CO on pathophysiology of heart failure, we performed the experiment on the HO-1 induction in the rat. Next, we tried to make heart failure model in rat, and to confirm the effect of the carbon monoxide. Finally the heart failure model was not accomplished though the induction of HO-1 succeeded. It is necessary to achieve complete heart failure model.
We performed another study on cytoprotective effects of CO. We found that CO protects isolated rat heart mitochondria and cultured cardiomyogenic cells from cyanide poisoning.
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