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Gas ¡í È£Èí ¡í ÀÏ»êÈ­Áú¼Ò

ÀÏ»êÈ­ Áú¼Ò  Nitric Oxide, NO

Áú¼Ò, Nitrogen source
- Áú¼Ò N2 gas
- Áú»ê NO3 : ´Ü¹éÁú
- ¾ÆÁú»ê NO2
- »êÈ­Áú¼Ò NO,¾Æ»êÈ­Áú¼Ò (N2O)
- Áú¼Ò¹èÃâ

½Å°æÀü´Þ¹°Áú : 2Â÷ Àü·É
- NO, CO
- cAMP,  Ä®½·
- wiki : NO - ¿ªÇÒ

- arginine

¡Ü »ý¼º°æ·Î



»êÈ­Áú¼Ò »ý¼º È¿¼Ò(NOS)
- nNOS : Neuronal NOS (nNOS)´Â ½Å°æÁ¶Á÷¿¡¼­ NO¸¦ »ý¼ºÇÏ¸ç ¼¼Æ÷°£ Åë½Å ±â´ÉÀÌ ÀÖ°í ¼¼Æ÷¸·°ú °ü·ÃÀÌ ÀÖ´Ù. nNOS ÀÛ¿ëÀº NPA (N-propyl-L-arginine)¿¡ ÀÇÇØ ¾ïÁ¦µÇ¸ç ÀÌ È¿¼Ò´Â 7-nitroindazole¿¡ ÀÇÇØ ¾ïÁ¦µÈ´Ù
- iNOS : Inducible NOS (iNOS)´Â ¸é¿ª°è¿¡ Á¸ÀçÇÏ¸ç ½ÉÇ÷°ü°è¿¡µµ ÀÖ´Ù. NOÀÇ »êÈ­ ½ºÆ®·¹½º ±â´ÉÀ» ÀÌ¿ëÇÏ¿© ´ë½Ä¼¼Æ÷°¡ º´¿øü¸¦ ÅðÄ¡ÇÒ ¶§ »ç¿ëÇÑ´Ù
- eNOS : Endothelial NOS (eNOS)´Â NOS3¶ó°í ¾Ë·ÁÁ® ÀÖ°í Ç÷°ü¿¡¼­ NO¸¦ »ý¼ºÇÏ¿© Ç÷°ü ±â´É¿¡ °ü¿©ÇÑ´Ù. constitutive Ca2+ ÀÇÁ¸ÀûÀÎ NOS(cNOS)´Â NOÀÇ ±âº»Àû ¹æÃâÀ» Á¦°øÇÏ¸ç ¼¼Æ÷¸·À̳ª °ñÁöü ¸·°ú ¿¬°üµÈ´Ù.


¡Ü ¿ªÇÒ : NO°¡ ¾Æ±ºÀ¸·Î È°¾àÇÒ ¶§



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-  Ç÷°ü ÆòÈ°±Ù Á¶Àý È¿°ú;¼Ò·®ÀÇ ÀûÀýÇÑ ºÐºñ,Àڱؿ¡¼­´Â Ç÷°üÈ®Àå È¿°ú·Î Ç÷·ù ¼øȯÀ» À¯Áö °³¼±½ÃŲ´Ù
-  ³ú½Å°æ ¼¼Æ÷°£ ±³ÅëÀ» Á¶ÀýÇÏ¿© ÁýÁß·Â, Á¤º¸ ÀÎ½Ä ±â´É, ±â¾ï·ÂÀ» °­È­
-  ¸é¿ª ¼¼Æ÷¿¡¼­ »ý¼ºµÈ NO´Â °¨¿°¿¡ ´ëÇ×ÇÏ°í Á¾¾ç¼¼Æ÷ Æı«, »óó Ä¡À¯ ±â´É °­È­
-  ¹ß±â ¹× ¼ºÀû ÈïºÐ °íÁ¶(Çظéü ³» Ç÷·ù À¯ÀÔ ±Ø´ëÈ­)
-  ¼ÒÈ­°ü ¿îµ¿ ±â´É È°¼ºÈ­ÇÏ¿© À½½Ä¹° ¼ÒÈ­±â´É °­È­

- ´©±¸´Â Ç÷°ü ÆØâ, Ç÷¾Ð °­ÇÏ & Á¤·ÂÁ¦¶ó°í Çϳ׿ä

³î¶ö ÀÏÀº ³²¼ºÀÇ ¼ºÀû ¹ß±â´Â NO·Î ½ÃÀ۵ȴٴ »ç½ÇÀÌ´Ù.
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Ç÷Áß »ê¼Ò ³óµµ°¡ ¶³¾îÁö¸é Ç÷°ü º®ÀÇ ³»ÇǼ¼Æ÷´Â ÀÏ»êÈ­ Áú¼Ò¸¦ »ý»êÇÑ´Ù. ÀÏ»êÈ­ Áú¼Ò´Â ÁÖº¯ÀÇ ±ÙÀ°¼¼Æ÷¿¡ ÀÛ¿ëÇÏ¿© ±ÙÀ°À» À̿ϽÃÅ°´Â È¿¼Ò¸¦ È°¼ºÈ­½ÃÄÑ Ç÷°üÀ» È®Àå½ÃÅ°´Â È¿°ú°¡ ÀÖ´Ù. Ç÷°üÀÌ È®ÀåµÈ °á°ú Á¶Á÷¿¡ »ê¼Ò°¡ ¿øÈ°ÇÏ°Ô °ø±ÞµÉ ¼ö ÀÖ°Ô µÈ´Ù. ±× ÈÄ ÀÏ»êÈ­ Áú¼Ò´Â ÀÛ¿ëÇÑÁö ¸î ÃÊ Áö³ªÁö ¾Ê¾Æ ºÐÇصȴÙ. ¶ÇÇÑ ÀÏ»êÈ­ Áú¼Ò´Â ³²¼ºÀÌ ¼ºÀûÀ¸·Î ÈïºÐÇÑ °æ¿ì ƯÁ¤ ½Å°æ ¼¼Æ÷·ÎºÎÅÍ »ý»êµÇ¾î ¹ß±âÁ¶Á÷ÀÇ Çظéü·Î ÅëÇÏ´Â Ç÷°üÀ» È®Àå½ÃÄÑ ¹ß±â¸¦ ÀÏÀ¸Å²´Ù. ÀÎü¿¡¼­ »ý±ä NO´Â GTP·ÎºÎÅÍ cGMPÀ» ¸¸µå´Â È¿¼Ò¸¦ È°¼ºÈ­½ÃŲ´Ù. cGMP¾çÀÌ ¸¹¾ÆÁö¸é ±Ù¼¼Æ÷ ¼ÓÀ¸·ÎºÎÅÍ Ä®½·ÀÌ¿ÂÀÌ ºüÁ®³ª¿À°Ô ÇϵçÁö ¾Æ´Ï¸é ¼¼Æ÷ ¼Ó ¾îµð¿£°¡ °¤ÇôÀÖ°Ô ÇÏ¿© ±ÙÀ°À» À̿ϽÃŲ´Ù. ³²¼º ¼º±â¿¡ ÀÖ´Â ½ºÆÝÁö ±ÙÀ° ¼¼Æ÷¿¡¼­ ÀÌ·± ÀÏÀÌ »ý±â¸é ´ç¿¬È÷ ±× Á¶Á÷¿¡ Ç÷¾×ÀÌ ½±°Ô Èê·¯ µé¾î°¡ ÆØÀ±½ÃŲ´Ù. ÀÌ¿Í °°Àº NOÀÇ ¿ªÇÒÀº ºñ±³Àû ÃÖ±ÙÀÎ 1991³â¿¡ ¹àÇôÁ³À¸¸ç ½º¿þµ§ ·éµå´ëÇÐ º´¿ø ¿¬±¸ÆÀ ´öºÐÀ̾ú´Ù.



Ç÷°üÀÌ NO¸¦ ¸¸µç´Ù´Â ¹ß°ßÀº 10¿©³â Àü ¿µ±¹ °úÇÐÀڵ鿡°Ô ÀÇÇØ ÀÌ·ç¾îÁ³À¸¸ç Ç÷°ü¿¡¼­ »ý±ä NO´Â ÀÎÁ¢ ±ÙÀ° ¼¼Æ÷¸¦ À̿ϽÃÄÑ Ç÷¾ÐÀ» ³·Ãá´Ù´Â °Íµµ ¾Ë°Ô µÇ¾ú´Ù. µû¶ó¼­ Çù½ÉÁõ ȯÀÚµéÀÌ ¸Ô´Â ¾ÆÁú»ê¾Æ¹Ð°ú ´ÏÆ®·Î±Û¸®¼¼¸°À¸·ÎºÎÅÍ NO°¡ »ý°Ü Ç÷°üÀ» È®Àå½ÃÄÑ Áֱ⠶§¹®¿¡ ÀÌ È­ÇÕ¹°ÀÌ È¯ÀÚ¸¦ À§Çè¿¡¼­ ¹þ¾î³ª°Ô ÇÑ´Ù´Â ¼³¸íÀÌ µÈ´Ù.  ¿ì¸® ÀÎü¿¡¼­ NO¸¦ ¸¸µå´Â È­ÇÕ¹°À» º¹¿ëÇϸç, À̵é·ÎºÎÅÍ »ý±ä NO´Â ÀÎü¿¡¼­ ¼öÃʹۿ¡ ¸Ó¹°Áö ¾Ê´Â´Ù. ±×·¯³ª ÀÌ ½Ã°£Àº ÀθíÀ» ±¸Çϱ⿡´Â ÃæºÐÈ÷ ±ä ½Ã°£ÀÌ´Ù. Á¤»óÀÎÀº ¾Æ¸£±â´ÑÀ̶ó´Â ¾Æ¹Ì³ë»êÀ¸·ÎºÎÅÍ NO¸¦ ¸¸µç´Ù. ¹°·Ð cGMP°¡ Ç׽à ¿ì¸® ¸ö¿¡ Ã游ÇØ ÀÖ´Ù¸é Æò»ó½Ã ³²¼ºµéÀÌ Áö³»±â ¸Å¿ì ºÒÆíÇÏ°ÚÀ¸³ª ´ÙÇàÈ÷ cGMP´Â Æ÷½ºÆ÷µð¿¡½ºÅ׶ó¾ÆÁ¦(PDE5)¶ó´Â È¿¼Ò¿¡ ÀÇÇØ ºÐÇصȴÙ. ºñ¾Æ±×¶óÀÇ À§·ÂÀÌ ¹Ù·Î ¿©±â¿¡ ÀÖ´Ù. ºñ¾Æ±×¶ó È­ÇÕ¹°Àº ±× ¸ð¾çÀÌ cGMP¿Í ¸Å¿ì À¯»çÇØ PDE5°¡ ±× Â÷À̸¦ ¾Ë¾Æº¸Áö ¸øÇÏ°í ¾óÅä´çÅä¾Ê°Ô ºñ¾Æ±×¶ó ºÐÀÚ¿¡ µé·¯ºÙ¾î º»¿¬ÀÇ ÀÓ¹«ÀÎ cGMP ºÐÇØ ´É·ÂÀ» ÀÒ°Ô ÇÑ´Ù. ÀÌ·¸°Ô µÇ¸é NO ´öºÐ¿¡ »ý±ä cGMP°¡ ¿À·¡ ¸Ó¹°°Ô µÇ¹Ç·Î Àå½Ã°£ ³²¼º ¼º±âÀÇ ¹ß±â¸¦ Áö¼ÓÇÒ ¼ö ÀÖ°Ô ÇÑ´Ù. ºñ¾Æ±×¶óÀÇ °æÀ̷οòÀº ¿ÏÀüÈ÷ ¿ì¿¬ÇÑ ¹ß°ßÀÇ ´öÀ̾ú´Ù. È­ÀÌÀڻ翡¼­´Â ÀÌ ¾àÀ» Çù½ÉÁõ Ä¡·áÁ¦·Î ½ÇÇèÇÏ°í ÀÖ¾ú´Âµ¥ ÀÌ»óÇÏ°Ôµµ ȯÀÚµéÀÌ Çù½ÉÁõ Ä¡·áº¸´Ù´Â ¼º»ýÈ° Çâ»óÀ» ´õ ÀÚ¶ûÇÏ´Â °ÍÀÌ ¾Æ´Ñ°¡... ½ÉÀå±ÙÀ°¿¡µµ PDE5 È¿¼Ò°¡ º°·Î ¾ø´Ù´Â °ÍÀ» ÁøÀÛ ¾Ë¾Ò´õ¶ó¸é ºñ¾Æ±×¶óÀÇ ½ÃÆÇÀº ÈξÀ »¡¶úÀ» Áöµµ ¸ð¸£´Â ÀÏÀÌ´Ù.

 


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¡Ü ¿ªÇÒ : NO°¡ Àû±ºÀÏ ¶§
-  Ç÷·ù È帧 ¹æÇØÇÏ¿© ½ÉÇ÷°ü°è, ³úÇ÷°ü°è Áúȯ À¯¹ß
-  ¸é¿ª¼¼Æ÷¿¡¼­ °úÀ× »ý¼º- °üÀý¿°, ¿°Áõ¼º ÀåÁúȯ µî ÀÚ°¡¸é¿ª Áúȯ, ¾Ï µî ¸¸¼º ¿°Áõ¼º Áúȯ À¯¹ß
-  °úÀ×»ý¼ºµÈ NO´Â ¼ö¸¹Àº free radical »ý¼ºÀ» ÃËÁø
-  ³ú½Å°æ°è¿¡ ÀÛ¿ëÇÏ¿© mental function ¹æÇØ·Î ±â¾ï·Â °¨¼Ò, ³ú ³ëÈ­ ÃÊ·¡

- ¾ÆÁú»ê : Çì¸ð±Û·Îºó°ú °áÇÕÇÏ¿© µ¶À̶ó´Â À̾߱⵵ ÀÖ°í
  
  ¾à 10¿©³â Àü¸¸ ÇÏ´õ¶óµµ nitric oxide(NO)´Â ´ÜÁö ÀÚµ¿Â÷³ª Ç×°ø±â¿¡¼­ ¹èÃâµÇ´Â ¹°Áú·Î¼­
  »ê¼ººñ¸¦ ÃÊ·¡Çϰųª ¿ÀÁ¸ÃþÀ» ºØ±«½ÃÅ°´Â µ¶¼ºÀÌ ¸Å¿ì °­ÇÑ °¡½º¼º ¹°Áú·Î¸¸ ¿©°å¾ú´Ù.

- ¼¼Æ÷Àڻ쿡¼­ ¿ªÇÒ
Nitric oxide (NO) is an important signaling molecule that acts in many tissues to regulate a diverse range of physiological processes including vasodilation, neuronal function, inflammation and immune function. Nitric oxide has also been demonstrated to be involved in the regulation of apoptosis.

The effects of apoptosis vary depending upon the dose of NO and the type of cell used and has been shown to be able to both induce apoptosis and to protect from apoptosis in different cell types. Nitric oxide has been demonstrated to inhibit apoptosis in a number of cell types including leukocytes, hepatocytes, trophoblasts and endothelial cells. Generally the anti-apoptotic effects of NO can be mediated through a number of mechanisms such as the nitrosylation and inactivation of many of the caspases including caspase 3, caspase 1 and caspase 8. Other mechanisms include activating p53, upregulating heat shock protein 70 (and consequently blocking recruitment of pro-caspase 9 to the Apaf-1 apoptosome), upregulating Bcl-2 and Bcl-XL (with subsequent inhibition of cytochrome C release from the mitochondria) and activating cGMP signaling leading to activation of cGMP-dependent protein kinases and suppression of caspase activity.

The effects of NO on apoptosis are generally classified as cGMP dependent or independent. Nitric oxide is able to activate cGMP signaling through the interaction of NO with the haem group of guanylate cyclase. The production of cGMP leads to the activation of cGMP-dependent protein kinases and possibly to increased expression of anti-apoptotic proteins. We are particularly interested in the anti-apoptotic effects of NO on endothelial cells and trophoblasts and are currently investigating the mechanism of action of NO in these cells.



 
 


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