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위점막의 산화성 손상에 대한 nitric oxide와 glutathione redox cycle의 세포 방어기전

Other Titles
 Antioxidative defense mechanism of nitric oxide and glutathione redox cycle in gastric mucosa 
Authors
 김문아 
Issue Date
1997
Description
의학과/박사
Abstract
[한글]

위점막은 위강내에서 생성되는 유해한 여러종류의 활성산소에 계속 노출되고 있다. Glutathione redox cycle은 H^^2 O^^2를 제거함으로써, 위점막의 항산화 방어기능을 나타낸다. Nioicoxide는 acetaminophen 유발 간손상에서 glutathione 항상성을 유지시켜 보호효과를 나타낸다. 본 연구에서는 H^^2 O^^2로 유발한 위점막세포 손상에서 nitric oxide와 glutathifnle redox cycle의 역할을 규명하고자 하였다 토끼의 위선세포를 신선하게 분리한 후, β-D-glucose와 glucose oxidase를 투여하여 H^^2 O^^2를 생성시킴으로써 위점막손상을 유발시켰다. Nitric oxide의 영향을 관찰하기 위하여 L-arginine, N**G -nitro-L-argin ine methyl ester 및 N**G-nitro-L-arginine을 glucose/glucose oxidase와 함께 투여하였다. Glutathione redox cycle의 영향은 glucose/glucose oxidase에 노출된 세포에 1-chloro-2,4- dinitrobenzene과 buthionine sulfoximine을 단독 또는 L-arginine과 병용투여하여 검색하였다. 배양이 끝난 후 배양액내 유리된 지질파산화물과 nitric oxide의 지표로 nitrite를 측정 하였으며, 세포내 glutathione 함량 및 glutathione peroxidase

활성을 측정하였다.

결과로서, glucose와 함께 투여한 glucose oxidase용량에 비례하여 위점막세포의 지질과산화물 생성은 증가하였고, nitrite, glutathione 함량 및 glutathione perDxidase 활성은 감소하였다. Nieic oxide synthase의 기질인 L-arginine의 전처치로 지질과산화물 생성 증가가 억제되었고, nitrite, glutathione 함량 및 glutathione peroxidase 활성 감소가 억제되었다. Nitric oxide synthase억제제인 N**G_nitro-L-arginine methyl ester 및 N**G -nitro-L-arginine은 H^^2 O^^2로 유발한 위점막세포손상에 대하여 보호 효과를 나타내지 않았다. Glucose/ glucose oxidate에 노출시킨 위점막세포에 L-arginine 단독

또는 glutathione redox cycle 억제제와 병용투여시 L-arginine은 glucose/glucose oxidase 또는 glutathione redox cycle 억제제로 인한 세포내 glutathione 함략의 감소를 방지 하였다.

결론적으로 nitric oxide는 H^^2 O^^2로 유발한 위점막 손상에 대하여 보호효과를 나타내며, 이는 nitric oxide가 지질과산화를 억제하고 세포내 glutathione 함량을 유지시키기 때문인 것으로 생각된다.



[영문]

Gastric mucosa is continuously exposed to toxic and reactive oxygen species generated within the lumen. Glutathione redox cycle removes H^^2 O^^2 and has a dominant antioxidant function in gastric cells. Nitric oxide is repgrted to protect acetaminophen-induced hepatotoxicity by maintaining glutathione homeostasis. The pesent study examined the iole of nitric oxide and glutathione iedox cycle in H^^2 O^^2 -induced damage of gastric cells. Freshly isolated gastric cells of rabbit

were used. β-D-Glucose and glucose oxidase reaction was used to generate H2O2 in H^^2 O^^2 -induced damage of gastric cells. L-Arginine, N**G -nitro-L-arginine methyl

ester, or N**G -nitrt-L-arg mine were added to the cells treated with glucose/glucose oxidise. 1-Chloro-2,4-dinitrobenzene and/ or buthionine sulfoximine were added to the cells exposed to glucose/glucose oxidate with or without L-arginine. Lipid peroxidation, cellular content of glutathione and the activity of

glutathione peroxidase were detennined. Nitrite was measured as an index of nitric oxide.

Dose-dependent increase in lipid peroxide production as well as dose-dependent decrease in nitrite, cellular glutathione content and glutathione peroxidase activity were observed in the cells treated with glucose/glucose oxidase. Pretreaunent with L-arginine, a substrate for nitric oxide synthase, prevented the

increase in lipid peroxide production and the reduction of nitrite as well as glutathione content and glutathione peroxidase activity. Inhibitors of nitric oxide synthase such as N**G -nitro-L-arginine methyl ester and N**G -nitro-L-arginine did not protect H^^2 O^^2-induced cell damage. L-arginine protected the deorease in glutathiene content of gastric cells induced by glucose glucose oxidase with or without glutathione redox cycle inhibitors.

In conclusion, it is suggested that nitric oxide protects gastric mucosal cells from H^^2 O^^2 possibly by inhibiting lipid peroxidation arid by preserving cellular glutathione stores.
Full Text
https://ymlib.yonsei.ac.kr/catalog/search/book-detail/?cid=CAT000000006591
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Appears in Collections:
1. College of Medicine (의과대학) > Others (기타) > 3. Dissertation
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/125503
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