Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.7.1.2 (nitrate reductase)
 3,861 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to investigate the change of aortic semicarbazide-sensitive amine oxidase (SSAO) activity in diabetic rats and examine the effect of 2-bromoethylamine (2-BEA) on SSAO activity and vascular endothelium in diabetic rats. SSAO was prepared from rat aorta. For assessment of the inhibitory effect, the enzymes were preincubated in the presence of different concentrations of 2-BEA before the addition of benzylamine in vitro. Type 1 diabetic rat model was induced by a single intraperitoneal injection of streptozotocin (STZ). Sprague Dawley (SD) rats were randomly divided into normal control group (NC), diabetic model group (DM), 2-BEA 5 mg/kg group, 2-BEA 20 mg/kg group (n = 10 in each group). 2-BEA was administered daily via intraperitoneal injection for 8 weeks. At the end of 8 weeks, blood sample was collected from the abdominal aorta. Plasma nitric oxide (NO) was determined by nitrate reductase method. Plasma endothelin-1 (ET-1) was determined by radioimmunoassay. Aorta SSAO was determined by high performance liquid chromatography. The aorta was prepared to observe morphological changes and ultramicroscopic structures. The results were as follows: Compared with NC group, aortic SSAO activity and the plasma ET-1 were significantly increased (P < 0.01), and plasma NO was significantly decreased (P < 0.01) in DM group. 2-BEA decreased plasma ET-1 and elevated plasma NO by inhibiting aortic SSAO activity in diabetic rats (P < 0.01), and 2-BEA 20 mg/kg group was more significant than 2-BEA 5 mg/kg group (P < 0.05). Endothelial injury of 2-BEA group rats was less serious than DM group. These results suggest that 2-BEA protect aortic endothelium by inhibiting aortic SSAO activity.
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PMID:[2-Bromoethylamine protects vascular endothelium by inhibiting SSAO activity in diabetic rats]. 2513 90

Nitric oxide (NO) is a key signaling molecule in plants, regulating a wide range of physiological processes. However, its origin in plants remains unclear. It can be generated from nitrite through a reductive pathway, notably via the action of the nitrate reductase (NR), and evidence suggests an additional oxidative pathway, involving arginine. From an initial screen of potential Arabidopsis thaliana mutants impaired in NO production, we identified copper amine oxidase 8 (CuAO8). Two cuao8 mutant lines displayed a decreased NO production in seedlings after elicitor treatment and salt stress. The NR-dependent pathway was not responsible for the impaired NO production as no change in NR activity was found in the mutants. However, total arginase activity was strongly increased in cuao8 knockout mutants after salt stress. Moreover, NO production could be restored in the mutants by arginase inhibition or arginine addition. Furthermore, arginine supplementation reversed the root growth phenotype observed in the mutants. These results demonstrate that CuAO8 participates in NO production by influencing arginine availability through the modulation of arginase activity. The influence of CuAO8 on arginine-dependent NO synthesis suggests a new regulatory pathway for NO production in plants.
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PMID:Copper amine oxidase 8 regulates arginine-dependent nitric oxide production in Arabidopsis thaliana. 2838 68