scholarly journals Effect of curcumin on the nitric oxide induced structural and functional modifications of high molecular mass goat brain cystatin

2010 ◽  
Vol 56 (2) ◽  
pp. 209-219
Author(s):  
S. Sumbul ◽  
M.S. Khan ◽  
B. Bano
Keyword(s):  
Nitric Oxide ◽  
Structural Damage ◽  
Proteinase Inhibitors ◽  
Cell Damage ◽  
Novel Drugs ◽  
Almost All ◽  
Antiproteolytic Activity ◽  
Neural Diseases ◽  
Goat Brain ◽  
Thiol Proteinase

Cystatins are thiol proteinase inhibitors ubiquitously present in the mammalian body. In brain, they prevent unwanted proteolysis and are involved in several neurodegenerative diseases. Under physiological conditions nitric oxide can be found in almost all the tissues, but under pathological conditions NO has damaging effects. Its increased concentration, under various neural diseases leads to cell damage through formation of highly reactive peroxynitrite. Our present study was designed to investigate the protective effect of curcumin against NO induced damage of HM-GBC. NO caused intensive structural and functional damage of HM-GBC, resulting in 89% loss of its antiproteolytic activity after 2 h of incubation. Structural damage occurs in the form of protein degradation. Curcumin significantly protected HM-GBC against this damage. This suggests that curcumin has a significant potential in the treatment of diseases caused by nitrogen free radicals and this potential must be further explored for the development of novel drugs.

Nitric Oxide in Life and Death of Neutrophils

2019 ◽  
Vol 26 (31) ◽  
pp. 5764-5780 ◽  
Author(s):  
Svetlana I. Galkina ◽  
Ekaterina A. Golenkina ◽  
Galina M. Viryasova ◽  
Yulia M. Romanova ◽  
Galina F. Sud’ina
Keyword(s):  
Nitric Oxide ◽  
Cell Damage ◽  
Protective Role ◽  
Neutrophil Apoptosis ◽  
High Biological Activity ◽  
Life And Death ◽  
Signalling Molecule ◽  
Activated Neutrophils ◽  
Cell Death Mechanisms ◽  
Prostacyclin Synthase

Background: Nitric Oxide (NO) is a key signalling molecule that has an important role in inflammation. It can be secreted by endothelial cells, neutrophils, and other cells, and once in circulation, NO plays important roles in regulating various neutrophil cellular activities and fate. Objective: To describe neutrophil cellular responses influenced by NO and its concomitant compound peroxynitrite and signalling mechanisms for neutrophil apoptosis. Methods: Literature was reviewed to assess the effects of NO on neutrophils. Results: NO plays an important role in various neutrophil cellular activities and interaction with other cells. The characteristic cellular activities of neutrophils are adhesion and phagocytosis. NO plays a protective role in neutrophil-endothelial interaction by preventing neutrophil adhesion and endothelial cell damage by activated neutrophils. NO suppresses neutrophil phagocytic activity but stimulates longdistance contact interactions through tubulovesicular extensions or cytonemes. Neutrophils are the main source of superoxide, but NO flow results in the formation of peroxynitrite, a compound with high biological activity. Peroxynitrite is involved in the regulation of eicosanoid biosynthesis and inhibits endothelial prostacyclin synthase. NO and peroxynitrite modulate cellular 5-lipoxygenase activity and leukotriene synthesis. Long-term exposure of neutrophils to NO results in the activation of cell death mechanisms and neutrophil apoptosis. Conclusion: Nitric oxide and the NO/superoxide interplay fine-tune mechanisms regulating life and death in neutrophils.

Enalapril attenuates cardiorenal damage in nitric-oxide-deficient spontaneously hypertensive rats

2004 ◽  
Vol 106 (3) ◽  
pp. 337-343 ◽  
Author(s):  
Leila M. M. PEREIRA ◽  
Daniele G. BEZERRA ◽  
Denise L. MACHADO ◽  
Carlos A. MANDARIM-DE-LACERDA
Keyword(s):  
Nitric Oxide ◽  
Body Mass ◽  
Structural Damage ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Genetic Hypertension ◽  
Lv Mass ◽  
Significant Difference

Stereological structural alterations of the heart and kidney were studied in four groups (n=5) of spontaneously hypertensive rats (SHRs) treated for 30 days: (i) control, (ii) NG-nitro-L-arginine methyl ester [L-NAME; nitric oxide (NO) synthesis inhibitor] alone, (iii) enalapril alone and (iv) L-NAME plus enalapril. Blood pressure (BP) was elevated significantly in NO-deficient SHRs (rats receiving L-NAME) or significantly lower in enalapril-treated SHRs. Co-administration of L-NAME and enalapril caused a 20% decrease in BP compared with untreated SHRs. NO-deficient SHRs had a decrease in body mass, but this loss of body mass was prevented efficiently in the enalapril-treated group. Enalapril treatment decreased the left ventricular (LV) mass index in SHRs, even in animals with NO synthesis blocked. NO deficiency in SHRs caused a larger decrease in the number of LV cardiomyocyte nuclei, which had a negative correlation with both LV mass index and BP. The volume-weighted glomerular volume (VWGV) separated the SHRs into two groupings: (i) control and NO-deficient SHRs, and (ii) enalapril- and L-NAME plus enalapril-treated SHRs. There was a significant difference between these two groupings, with VWGV being more than 15% smaller in the latter compared with the former grouping. The present findings reinforce the evidence that enalapril efficiently treats genetic hypertension, and demonstrate that this effect is observed even when NO synthesis is inhibited. Enalapril administration also decreases cardiac and renal structural damage caused by genetic hypertension, as well as by the interaction between genetic hypertension and NO deficiency.

scholarly journals Gaseous neurotransmitter nitric oxide: Its role in experimental models of epilepsy

2012 ◽  
Vol 64 (3) ◽  
pp. 1207-1216 ◽  
Author(s):  
D. Hrncic ◽  
Aleksandra Rasic-Markovic ◽  
Jelica Bjekic-Macut ◽  
Veselinka Susic ◽  
D. Mladenovic ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Experimental Studies ◽  
Experimental Models ◽  
Initiation And Propagation ◽  
Organ Systems ◽  
The Central Nervous System ◽  
Animal Models Of Epilepsy ◽  
Almost All ◽  
Gaseous Neurotransmitter ◽  
Models Of Epilepsy

Epilepsy is one of the leading neurological disorders and affects 1-2% of the world?s population. Generally, it is a result of an imbalance between excitatory and inhibitory phenomena in the central nervous system (CNS), but the mechanisms of its initiation and propagation still require further investigations. Experimental models represent one of the most powerful tools to better understand the mechanisms of epileptogenesis. Nitric oxide (NO) is gaseous molecule with pleiotropic physiological and pathological effects in almost all organ systems and intriguing biological relevance, especially in the CNS where it acts as a gaseous neurotransmitter. The role of NO in the generation of epilepsy is highly contradictory, since there is evidence of its anticonvulsive, as well as proconvulsive properties. Therefore, we will discuss in this review the involvement of NO-mediated signaling pathways in the mechanisms of epileptogenesis, taking into account the findings revealed in experimental studies on animal models of epilepsy.

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 Iodinated contrast media cause direct tubular cell damage, leading to oxidative stress, low nitric oxide, and impairment of tubuloglomerular feedback

2014 ◽  
Vol 306 (8) ◽  
pp. F864-F872 ◽  
Author(s):  
Zhi Zhao Liu ◽  
Kristin Schmerbach ◽  
Yuan Lu ◽  
Andrea Perlewitz ◽  
Tatiana Nikitina ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Trypan Blue ◽  
Cell Damage ◽  
Kidney Injury ◽  
Tubuloglomerular Feedback ◽  
Iodinated Contrast Media ◽  
Expression Of Genes ◽  
Iodinated Contrast ◽  
Direct Cell

Iodinated contrast media (CM) have adverse effects that may result in contrast-induced acute kidney injury. Oxidative stress is believed to play a role in CM-induced kidney injury. We test the hypothesis that oxidative stress and reduced nitric oxide in tubules are consequences of CM-induced direct cell damage and that increased local oxidative stress may increase tubuloglomerular feedback. Rat thick ascending limbs (TAL) were isolated and perfused. Superoxide and nitric oxide were quantified using fluorescence techniques. Cell death rate was estimated using propidium iodide and trypan blue. The function of macula densa and tubuloglomerular feedback responsiveness were measured in isolated, perfused juxtaglomerular apparatuses (JGA) of rabbits. The expression of genes related to oxidative stress and the activity of superoxide dismutase (SOD) were investigated in the renal medulla of rats that received CM. CM increased superoxide concentration and reduced nitric oxide bioavailability in TAL. Propidium iodide fluorescence and trypan blue uptake increased more in CM-perfused TAL than in controls, indicating increased rate of cell death. There were no marked acute changes in the expression of genes related to oxidative stress in medullary segments of Henle's loop. SOD activity did not differ between CM and control groups. The tubuloglomerular feedback in isolated JGA was increased by CM. Tubular cell damage and accompanying oxidative stress in our model are consequences of CM-induced direct cell damage, which also modifies the tubulovascular interaction at the macula densa, and may therefore contribute to disturbances of renal perfusion and filtration.

Different Tissue Distributions of Two Types of Thiol Proteinase Inhibitors from Rat Liver and Epidermis1

1984 ◽  
Vol 96 (5) ◽  
pp. 1437-1442 ◽  
Author(s):  
Eiki KOMINAMI ◽  
Yoshiaki BANDO ◽  
Nobuaki WAKAMATSU ◽  
Nobuhiko KATUNUMA
Keyword(s):  
Rat Liver ◽  
Proteinase Inhibitors ◽  
Thiol Proteinase

scholarly journals Renal ischemia in the rat stimulates glomerular nitric oxide synthesis

2001 ◽  
Vol 280 (3) ◽  
pp. R771-R779 ◽  
Author(s):  
José M. Valdivielso ◽  
Carlos Crespo ◽  
José R. Alonso ◽  
Carlos Martı́nez-Salgado ◽  
Nelida Eleno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Structural Damage ◽  
Renal Damage ◽  
Protective Role ◽  
Renal Ischemia ◽  
No Production ◽  
Ischemia And Reperfusion ◽  
Nitric Oxide Synthesis ◽  
Cgmp Production ◽  
Synthesis Activity

Renal ischemia in humans and in experimental animals is associated with a complex and possibly interrelated series of events. In this study, we have investigated the glomerular nitric oxide (NO) production after renal ischemia. Unilateral or bilateral renal ischemia was induced in Wistar rats by clamping one or both renal arteries. NO production was assessed by measuring glomerular production of nitrite, a stable end product of NO catabolism, and NO-dependent glomerular cGMP production and by assessing the glomerular NADPH diaphorase (ND) activity, an enzymatic activity that colocalizes with NO-synthesis activity. Furthermore, we determined the isoform of NO synthase (NOS) implicated in NO synthesis by Western blot and immunohistochemistry. Glomeruli from rats with bilateral ischemia showed elevated glomerular nitrite and cGMP production. Besides, glomeruli from this group of rats showed an increased ND activity, whereas glomeruli from the ischemic and nonischemic rats with unilateral ischemia did not show this increase in nitrite, cGMP, and ND activity. In addition, glomeruli from ischemic kidneys showed an increased expression of endothelial NOS without changes in the inducible isoform. Addition ofl-NAME in the drinking water induced a higher increase in the severity of the functional and structural damage in rats with bilateral ischemia than in rats with unilateral ischemia and in sham-operated animals. We can conclude that after renal ischemia, there is an increased glomerular NO synthesis subsequent to an activation of endothelial NOS that plays a protective role in the renal damage induced by ischemia and reperfusion.

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