Nitric oxide and oxygen metabolism in inflammatory conditions: sepsis and exposition to polluted ambients

10.2741/2117 ◽  
2007 ◽  
Vol 12 (1) ◽  
pp. 964 ◽  
Author(s):  
Silvia Alvarez
Keyword(s):  
Nitric Oxide ◽  
Oxygen Metabolism ◽  
Inflammatory Conditions

scholarly journals Characterization of the Oxidative Stress in Renal Ischemia/Reperfusion-Induced Cardiorenal Syndrome Type 3

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Wellington Caio-Silva ◽  
Danielle da Silva Dias ◽  
Carolina Victoria Cruz Junho ◽  
Karine Panico ◽  
Raquel Silva Neres-Santos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Cardiorenal Syndrome ◽  
Redox Balance ◽  
Renal Ischemia ◽  
Cellular Damage ◽  
Cellular Mechanisms ◽  
Inflammatory Conditions

In kidney disease (KD), several factors released into the bloodstream can induce a series of changes in the heart, leading to a wide variety of clinical situations called cardiorenal syndrome (CRS). Reactive oxygen species (ROS) play an important role in the signaling and progression of systemic inflammatory conditions, as observed in KD. The aim of the present study was to characterize the redox balance in renal ischemia/reperfusion-induced cardiac remodeling. C57BL/6 male mice were subjected to occlusion of the left renal pedicle, unilateral, for 60 min, followed by reperfusion for 8 and 15 days, respectively. The following redox balance components were evaluated: catalase (CAT), superoxide dismutase (SOD), total antioxidant capacity (FRAP), NADPH oxidase (NOX), nitric oxide synthase (NOS), hydrogen peroxide (H2O2), and the tissue bioavailability of nitric oxide (NO) such as S-nitrosothiol (RSNO) and nitrite (NO2−). The results indicated a process of renoprotection in both kidneys, indicated by the reduction of cellular damage and some oxidant agents. We also observed an increase in the activity of antioxidant enzymes, such as SOD, and an increase in NO bioavailability. In the heart, we noticed an increase in the activity of NOX and NOS, together with increased cell damage on day 8, followed by a reduction in protein damage on day 15. The present study concludes that the kidneys and heart undergo distinct processes of damage and repair at the analyzed times, since the heart is a secondary target of ischemic kidney injury. These results are important for a better understanding of the cellular mechanisms involved in CRS.

scholarly journals A.361 Influence of inhaled nitric oxide on tissue oxygen metabolism

1996 ◽  
Vol 76 ◽  
pp. 112
Author(s):  
A. De Sio ◽  
E. De Biasio ◽  
A. Papa ◽  
D. Golia
Keyword(s):  
Nitric Oxide ◽  
Oxygen Metabolism ◽  
Inhaled Nitric Oxide ◽  
Tissue Oxygen

scholarly journals Oxygen Metabolism by Endothelial Nitric-oxide Synthase

2007 ◽  
Vol 282 (39) ◽  
pp. 28557-28565 ◽  
Author(s):  
Ying Tong Gao ◽  
Linda J. Roman ◽  
Pavel Martásek ◽  
Satya Prakash Panda ◽  
Yuzuru Ishimura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxygen Metabolism ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Kininase I-type carboxypeptidases enhance nitric oxide production in endothelial cells by generating bradykinin B1receptor agonists

2003 ◽  
Vol 284 (6) ◽  
pp. H1959-H1968 ◽  
Author(s):  
Sakonwun Sangsree ◽  
Viktor Brovkovych ◽  
Richard D. Minshall ◽  
Randal A. Skidgel
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Interferon Γ ◽  
Linear Increase ◽  
Interleukin 1Β ◽  
No Production ◽  
Fourfold Increase ◽  
Receptor Agonists ◽  
Inflammatory Conditions ◽  
Golgi Region

Kininase I-type carboxypeptidases convert native kinin agonists for B2receptors into B1receptor agonists by specifically removing the COOH-terminal Arg residue. The membrane localization of carboxypeptidase M (CPM) and carboxypeptidase D (CPD) make them ideally situated to regulate kinin activity. Nitric oxide (NO) release from human lung microvascular endothelial cells (HLMVEC) was measured directly in real time with a porphyrinic microsensor. Bradykinin (1–100 nM) elicited a transient (5 min) peak of generation of NO that was blocked by the B2antagonist HOE 140, whereas B1agonist des-Arg10-kallidin caused a small linear increase in NO over 20 min. Treatment of HLMVEC with 5 ng/ml interleukin-1β and 200 U/ml interferon-γ for 16 h upregulated B1receptors as shown by an approximately fourfold increase in prolonged (>20 min) output of NO in response to des-Arg10-kallidin, which was blocked by the B1antagonist des-Arg10-Leu9-kallidin. B2receptor agonists bradykinin or kallidin also generated prolonged NO production in treated HLMVEC, which was significantly reduced by either a B1antagonist or carboxypeptidase inhibitor, and completely abolished with a combination of B1and B2receptor antagonists. Furthermore, CPM and CPD activities were increased about twofold in membrane fractions of HLMVEC treated with interleukin-1β and interferon-γ compared with control cells. Immunostaining localized CPD primarily in a perinuclear/Golgi region, whereas CPM was on the cell membrane. These data show that cellular kininase I-type carboxypeptidases can enhance kinin signaling and NO production by converting B2agonists to B1agonists, especially in inflammatory conditions.

Hepatic oxygen metabolism in porcine endotoxemia: the effect of nitric oxide synthase inhibition

1998 ◽  
Vol 275 (6) ◽  
pp. G1377-G1385 ◽  
Author(s):  
Torunn Saetre ◽  
Yngvar Gundersen ◽  
Otto A. Smiseth ◽  
Tim Scholz ◽  
Hege Carlsen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxygen Delivery ◽  
Statistical Significance ◽  
Liver Blood Flow ◽  
Oxygen Metabolism ◽  
Extraction Ratio ◽  
Oxygen Extraction ◽  
Oxygen Extraction Ratio ◽  
Circulatory Effects ◽  
Hepatic Oxygen Delivery

The role of endotoxin (lipopolysaccharide, LPS) and nitric oxide in hepatic oxygen metabolism was investigated in 36 pigs receiving 1) LPS (1.7 μg ⋅ kg−1 ⋅ h−1) for 7 h and N G-nitro-l-arginine methyl ester (l-NAME; 25 mg/kg) after 3 h, 2) LPS, 3) NaCl andl-NAME, and 4) NaCl. Infusion of LPS reduced hepatic oxygen delivery (Do 2H) from 60 ± 4 to 30 ± 5 ml/min ( P < 0.05) and increased the oxygen extraction ratio from 0.29 ± 0.07 to 0.68 ± 0.04 after 3 h ( P < 0.05). Hepatic oxygen consumption (V˙o 2H) was maintained (18 ± 4 and 21 ± 4 ml/min, change not significant), but acidosis developed. Administration ofl-NAME during endotoxemia caused further reduction of Do 2H from 30 ± 3 to 13 ± 2 ml/min ( P < 0.05) and increased hepatic oxygen extraction ratio from 0.46 ± 0.04 to 0.80 ± 0.03 ( P< 0.05). There was a decrease inV˙o 2H from 13 ± 2 to 9 ± 2 ml/min that did not reach statistical significance, probably representing a type II error. Acidosis was aggravated. Administration of l-NAME in the absence of endotoxin also increased the hepatic oxygen extraction ratio, but no acidosis developed. In a different experiment, liver blood flow was mechanically reduced in the presence and absence of endotoxin, comparable to the flow reductions caused byl-NAME. The increase in hepatic oxygen extraction ratio (0.34) and maximum hepatic oxygen extraction ratio (∼0.90) was similar whether Do 2H was reduced by occlusion or byl-NAME. We concluded thatl-NAME has detrimental circulatory effects in this model. However, neither endotoxin norl-NAME seemed to prevent the ability of the still circulated parts of the liver to increase hepatic oxygen extraction ratio to almost maximum when oxygen delivery was reduced. The effect of l-NAME on oxygen transport thus seems to be caused by a reduction in Do 2H rather than by alterations in oxygen extraction capabilities.

scholarly journals Plant Peroxisomes, Reactive Oxygen Metabolism and Nitric Oxide

IUBMB Life ◽  
2008 ◽  
Vol 55 (2) ◽  
pp. 71-81 ◽  
Author(s):  
Luis A. Del Río ◽  
F. Javier Corpas ◽  
Luisa M. Sandalio ◽  
José M. Palma ◽  
Juan B. Barroso
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Reactive Oxygen Metabolism
Sign in / Sign up

Export Citation Format

Share Document