Deciphering the Protective Role of Nitric Oxide against Salt Stress at the Physiological and Proteomic Levels in Maize

In these studies we investigated if losartan, an AT1- receptor blocker has any beneficial effect on NO production from the bovine aortic preparations in vitro while under stimulation from angiotensin II. Experiments were performed on intact specimens of bovine thoracic aorta, incubated in Dulbeco's MOD medium in a metabolic shaker for 24 hours under 95 % O2 and 5 % CO2 at a temperature of 37°C. We found that angiotensin II 1nM−10 μM does not exert any statistically significant action on NO production. On the contrary, angiotensin II 10nM increases the production of NO by 58.14 % (from 12.16 + 2.9 μm/l to 19.23 + 4.2 μm/l in the presence of losartan 1nM (P<0.05). Nitric oxide levels depend on both rate production and rate catabolism or chemical inactivation. Such an equilibrium is vital for the normal function of many systems including the cardiovascular one. The above results demonstrate that the blockade of AT1-receptors favors the biosynthesis of NO and indicate the protective role of losartan on the vascular wall.

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Protective Role of Inhaled Nitric Oxide in Ischemia/Reperfusion and Endotoxin-Induced Inflammation

Yearbook of Intensive Care and Emergency Medicine - Yearbook of Intensive Care and Emergency Medicine 1999 ◽

10.1007/978-3-662-13453-5_36 ◽

1999 ◽

pp. 406-414

Author(s):

R. Nevière ◽

B. Guery

Keyword(s):

Nitric Oxide ◽

Ischemia Reperfusion ◽

Protective Role ◽

Inhaled Nitric Oxide

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Nitric Oxide Does Not Inhibit but Is Metabolized by the Cytochrome bcc-aa3 Supercomplex

International Journal of Molecular Sciences ◽

10.3390/ijms21228521 ◽

2020 ◽

Vol 21 (22) ◽

pp. 8521 ◽

Cited By ~ 1

Author(s):

Elena Forte ◽

Alessandro Giuffrè ◽

Li-shar Huang ◽

Edward A. Berry ◽

Vitaliy B. Borisov

Keyword(s):

Nitric Oxide ◽

Active Site ◽

Protective Role ◽

Terminal Oxidase ◽

O2 Consumption ◽

Turnover Number ◽

Terminal Oxidases ◽

Reducing Conditions ◽

No Consumption

Nitric oxide (NO) is a well-known active site ligand and inhibitor of respiratory terminal oxidases. Here, we investigated the interaction of NO with a purified chimeric bcc-aa3 supercomplex composed of Mycobacterium tuberculosis cytochrome bcc and Mycobacterium smegmatisaa3-type terminal oxidase. Strikingly, we found that the enzyme in turnover with O2 and reductants is resistant to inhibition by the ligand, being able to metabolize NO at 25 °C with an apparent turnover number as high as ≈303 mol NO (mol enzyme)−1 min−1 at 30 µM NO. The rate of NO consumption proved to be proportional to that of O2 consumption, with 2.65 ± 0.19 molecules of NO being consumed per O2 molecule by the mycobacterial bcc-aa3. The enzyme was found to metabolize the ligand even under anaerobic reducing conditions with a turnover number of 2.8 ± 0.5 mol NO (mol enzyme)−1 min−1 at 25 °C and 8.4 µM NO. These results suggest a protective role of mycobacterial bcc-aa3 supercomplexes against NO stress.

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Role of nitric oxide in hepatic microvascular injury elicited by acetaminophen in mice

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00217.2003 ◽

2004 ◽

Vol 286 (1) ◽

pp. G60-G67 ◽

Cited By ~ 48

Author(s):

Yoshiya Ito ◽

Edward R. Abril ◽

Nancy W. Bethea ◽

Robert S. McCuskey

Keyword(s):

Nitric Oxide ◽

Liver Injury ◽

Cell Injury ◽

Parenchymal Cell ◽

Protective Role ◽

Hepatic Expression ◽

Inos Inhibitor ◽

Microcirculatory Disturbances

Nitric oxide (NO) is suggested to play a role in liver injury elicited by acetaminophen (APAP). Hepatic microcirculatory dysfunction also is reported to contribute to the development of the injury. As a result, the role of NO in hepatic microcirculatory alterations in response to APAP was examined in mice by in vivo microscopy. A selective inducible NO synthase (iNOS) inhibitor,l- N6-(1-iminoethyl)-lysine (l-NIL), or a nonselective NOS inhibitor, NG-nitro-l-arginine methyl ester (l-NAME), was intraperitoneally administered to animals 10 min before APAP gavage. l-NIL suppressed raised alanine aminotransferase (ALT) values 6 h after APAP, whereas l-NAME increased those 1.7-fold. Increased ALT levels were associated with hepatic expression of iNOS. l-NIL, but not l-NAME, reduced the expression. APAP caused a reduction (20%) in the numbers of perfused sinusoids. l-NIL restored the sinusoidal perfusion, but l-NAME was ineffective. APAP increased the area occupied by infiltrated erythrocytes into the extrasinusoidal space. l-NIL tended to minimize this infiltration, whereas l-NAME further enhanced it. APAP caused an increase (1.5-fold) in Kupffer cell phagocytic activity. This activity in response to APAP was blunted by l-NIL, whereas l-NAME further elevated it. l-NIL suppressed APAP-induced decreases in hepatic glutathione levels. These results suggest that NO derived from iNOS contributes to APAP-induced parenchymal cell injury and hepatic microcirculatory disturbances. l-NIL exerts preventive effects on the liver injury partly by inhibiting APAP bioactivation. In contrast, NO derived from constitutive isoforms of NOS exerts a protective role in liver microcirculation against APAP intoxication and thereby minimizes liver injury.

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