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EPR characterization of molecular targets for NO in mammalian cells and organelles.哺乳动物细胞和细胞器中一氧化氮分子靶点的电子顺磁共振波谱表征
FASEB J. 1993 Sep;7(12):1124-34. doi: 10.1096/fasebj.7.12.8397130.
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The reaction of no with superoxide.一氧化氮与超氧化物的反应。
Free Radic Res Commun. 1993;18(4):195-9. doi: 10.3109/10715769309145868.
3
Pathological implications of nitric oxide, superoxide and peroxynitrite formation.一氧化氮、超氧化物和过氧亚硝酸盐形成的病理意义。
Biochem Soc Trans. 1993 May;21(2):330-4. doi: 10.1042/bst0210330.
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Nitric oxide mediates Kupffer cell-induced reduction of mitochondrial energization in hepatoma cells: a comparison with oxidative burst.一氧化氮介导库普弗细胞诱导的肝癌细胞线粒体能量化减少:与氧化爆发的比较。
Cancer Res. 1993 Jun 1;53(11):2676-82.
5
Enzyme linked immunosorbent assay (ELISA) and immunoprecipitation studies on anti-goblet cell antibody using a mucin producing cell line in patients with inflammatory bowel disease.在炎症性肠病患者中,利用产生粘蛋白的细胞系对杯状细胞抗体进行酶联免疫吸附测定(ELISA)和免疫沉淀研究。
Gut. 1994 Feb;35(2):224-30. doi: 10.1136/gut.35.2.224.
6
Cytokines in intestinal inflammation: pathophysiological and clinical considerations.肠道炎症中的细胞因子:病理生理学及临床考量
Gastroenterology. 1994 Feb;106(2):533-9. doi: 10.1016/0016-5085(94)90614-9.
7
Increased nitric oxide synthesis in ulcerative colitis.溃疡性结肠炎中一氧化氮合成增加。
Lancet. 1993 Feb 20;341(8843):465-6. doi: 10.1016/0140-6736(93)90211-x.
8
Greatly increased luminal nitric oxide in ulcerative colitis.溃疡性结肠炎中管腔一氧化氮大幅增加。
Lancet. 1994 Dec 17;344(8938):1673-4. doi: 10.1016/s0140-6736(94)90460-x.
9
Spontaneous intestinal inflammation and nitric oxide metabolism in HLA-B27 transgenic rats.HLA - B27转基因大鼠的自发性肠道炎症与一氧化氮代谢
Gastroenterology. 1995 Jul;109(1):142-50. doi: 10.1016/0016-5085(95)90279-1.
10
Evidence for in vivo peroxynitrite production in human acute lung injury.人体急性肺损伤中体内过氧亚硝酸盐生成的证据。
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活动性溃疡性结肠炎患者结肠黏膜中诱导型一氧化氮合酶异构体表达增加及过氧亚硝酸盐的形成。

Increased expression of an inducible isoform of nitric oxide synthase and the formation of peroxynitrite in colonic mucosa of patients with active ulcerative colitis.

作者信息

Kimura H, Hokari R, Miura S, Shigematsu T, Hirokawa M, Akiba Y, Kurose I, Higuchi H, Fujimori H, Tsuzuki Y, Serizawa H, Ishii H

机构信息

Department of Internal Medicine, School of Medicine, Keio University, Tokyo, 160, Japan.

出版信息

Gut. 1998 Feb;42(2):180-7. doi: 10.1136/gut.42.2.180.

DOI:10.1136/gut.42.2.180
PMID:9536941
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1727005/
Abstract

BACKGROUND

Increased production of reactive metabolites of oxygen and nitrogen has been implicated in chronic inflammation of the gut. The object of this study was to examine the magnitude and location of nitric oxide synthase (NOS) activity and peroxynitrite formation in the colonic mucosa of patients with ulcerative colitis in relation to the degree of inflammation.

SUBJECTS

Thirty three patients with active ulcerative colitis (17 with mild or moderate inflammation, 16 with severe inflammation).

METHODS

Inducible NOS activity was determined in the colonic mucosa by measuring the conversion of L-arginine to citrulline in the absence of calcium. The localisation of NOS and nitrotyrosine immunoreactivity was assessed immunohistochemically using the labelled streptavidin biotin method.

RESULTS

Inducible NOS activity increased in parallel with the degree of inflammation of the mucosa. Expression of inducible NOS was found not only in the lamina propria, but also in the surface of the epithelium. Peroxynitrite formation as assessed by nitrotyrosine staining was frequently observed in the lamina propria of actively inflamed mucosa.

CONCLUSIONS

Nitric oxide and peroxynitrite formation may play an important role in causing irreversible cellular injury to the colonic mucosa in patients with active ulcerative colitis.

摘要

背景

氧和氮的反应性代谢产物生成增加与肠道慢性炎症有关。本研究的目的是检测溃疡性结肠炎患者结肠黏膜中一氧化氮合酶(NOS)活性和过氧亚硝酸盐形成的程度及位置,并探讨其与炎症程度的关系。

研究对象

33例活动期溃疡性结肠炎患者(17例轻度或中度炎症,16例重度炎症)。

方法

通过测量无钙条件下L-精氨酸向瓜氨酸的转化来测定结肠黏膜中的诱导型NOS活性。采用标记链霉亲和素生物素法免疫组化评估NOS和硝基酪氨酸免疫反应性的定位。

结果

诱导型NOS活性与黏膜炎症程度平行增加。诱导型NOS不仅在固有层表达,也在上皮表面表达。通过硝基酪氨酸染色评估,过氧亚硝酸盐形成在活动期炎症黏膜的固有层中经常观察到。

结论

一氧化氮和过氧亚硝酸盐的形成可能在活动期溃疡性结肠炎患者结肠黏膜不可逆细胞损伤中起重要作用。