Cytokine-induced nitric oxide induces mitochondrial dysfunction and cardiac depression in endotoxin-treated rat hearts

1998 ◽  
Vol 4 (3) ◽  
pp. 113
Author(s):  
Kazuko Akashi ◽  
Tetsuya Tatsumi ◽  
Natsuya Keira ◽  
Jun Shiraishi ◽  
Satoaki Matoba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Dysfunction ◽  
Cardiac Depression ◽  
Rat Hearts

Nitric oxide-cGMP pathway is involved in endotoxin-induced contractile dysfunction in rat hearts

2004 ◽  
Vol 96 (3) ◽  
pp. 853-860 ◽  
Author(s):  
Tetsuya Tatsumi ◽  
Natsuya Keira ◽  
Kazuko Akashi ◽  
Miyuki Kobara ◽  
Satoaki Matoba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylate Cyclase ◽  
Myocardial Dysfunction ◽  
Significant Negative Correlation ◽  
Left Ventricular ◽  
No Production ◽  
Contractile Dysfunction ◽  
Cardiac Depression ◽  
Rat Hearts ◽  
Developed Pressure

The mechanisms by which endotoxemia causes cardiac depression have not been fully elucidated. The present study examined the involvement of nitric oxide (NO) in this pathology. Rats were infused with lipopolysaccharide (LPS) or saline, and the plasma and myocardial [Formula: see text] and [Formula: see text] (NOx) concentrations were measured before or 3, 6, and 24 h after treatment. The hearts were then immediately isolated and mounted in a Langendorff apparatus, and left ventricular developed pressure (LVDP) was determined before biochemical analysis of the myocardium. LPS injection effected the expression of inducible NO synthase (iNOS) in the myocardium, a marked increase in plasma and myocardial NOx levels, and a significant decline in LVDP compared with saline controls. The LPS-induced NO production and concomitant cardiac depression were most pronounced 6 h after LPS injection and were accompanied by a significant increase in myocardial cGMP content. Myocardial ATP levels were not significantly altered after LPS injection. Significant negative correlation was observed between LVDP and myocardial cGMP content, as well as between LVDP and plasma NOx levels. Aminoguanidine, an inhibitor of iNOS, significantly attenuated the LPS-induced NOx production and contractile dysfunction. Furthermore, 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one, an inhibitor of soluble guanylate cyclase, significantly decreased myocardial cGMP content and attenuated the contractile depression, although aminoguanidine or 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one was not able to completely reverse myocardial dysfunction. Our data suggest that endotoxin-induced contractile dysfunction in rat hearts is associated with NO production by myocardial iNOS and a concomitant increase in myocardial cGMP.

Changes in Arginase-Nitric Oxide Synthase System at Adaptation to Prolonged Exercise Training by Swimming in Adult and Aged Rat Hearts

2012 ◽  
Vol 3 (4) ◽  
pp. 299-308 ◽  
Author(s):  
Anatolii V. Kotsuruba ◽  
Yulia P. Korkach ◽  
Sergey O. Talanov ◽  
Olga V. Bazilyuk ◽  
Lyubov G. Stepanenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Exercise Training ◽  
Prolonged Exercise ◽  
Aged Rat ◽  
Rat Hearts ◽  
Oxide Synthase

Role of nitric oxide-induced mtDNA damage in mitochondrial dysfunction and apoptosis

2006 ◽  
Vol 40 (5) ◽  
pp. 754-762 ◽  
Author(s):  
Lyudmila I. Rachek ◽  
Valentina I. Grishko ◽  
Susan P. LeDoux ◽  
Glenn L. Wilson
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Dysfunction ◽  
Mtdna Damage

scholarly journals Pleurotus albidus Modulates Mitochondrial Metabolism Disrupted by Hyperglycaemia in EA.hy926 Endothelial Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Gabriela Gambato ◽  
Elisa Maria Pavão ◽  
Gabriela Chilanti ◽  
Roselei Claudete Fontana ◽  
Mirian Salvador ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Mitochondrial Dysfunction ◽  
Complex I ◽  
Electron Transport Chain ◽  
Mitochondrial Disorder ◽  
Antioxidant Enzyme Activities ◽  
Ros Production ◽  
Oxygen Species ◽  
Transport Chain

Hyperglycaemia exacerbates the production of reactive oxygen species (ROS), contributing to the multiple complications associated with diabetes. Mitochondrial dysfunction is also known to be associated with diabetes. Therefore, the aim of this work was to study the effect of Pleurotus albidus extract on the mitochondrial dysfunction induced by hyperglycaemia in EA.hy926 endothelial cells. The results showed that P. albidus treatment prevented the increase in the activity of complex I of the electron transport chain and minimized the ROS production induced by hyperglycaemia. In addition, the extract minimized oxidative damage to lipids and proteins, caused an imbalance in the antioxidant enzyme activities of superoxide dismutase and catalase, and decreased the nitric oxide levels induced by hyperglycaemia. These data contribute to our understanding of the mitochondrial disorder induced by hyperglycaemia as well as establishing the conditions required to minimize these alterations.

Oxidative stress and diabetic cardiovascular disorders: roles of mitochondria and NADPH oxidaseThis review is one of a selection of papers published in a Special Issue on Oxidative Stress in Health and Disease.

2010 ◽  
Vol 88 (3) ◽  
pp. 241-248 ◽  
Author(s):  
Garry X. Shen
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Mitochondrial Dysfunction ◽  
Cardiovascular Complications ◽  
Hypoglycemic Agents ◽  
Diabetic Patients ◽  
Plasminogen Activator Inhibitor 1 ◽  
In Cells

Cardiovascular diseases are the predominant cause of death in patients with diabetes mellitus. Underlying mechanism for the susceptibility of diabetic patients to cardiovascular diseases remains unclear. Elevated oxidative stress was detected in diabetic patients and in animal models of diabetes. Hyperglycemia, oxidatively modified atherogenic lipoproteins, and advanced glycation end products are linked to oxidative stress in diabetes. Mitochondria are one of major sources of reactive oxygen species (ROS) in cells. Mitochondrial dysfunction increases electron leak and the generation of ROS from the mitochondrial respiratory chain (MRC). High levels of glucose and lipids impair the activities of MRC complex enzymes. NADPH oxidase (NOX) generates superoxide from NADPH in cells. Increased NOX activity was detected in diabetic patients. Hyperglycemia and hyperlipidemia increased the expression of NOX in vascular endothelial cells. Accumulated lines of evidence indicate that oxidative stress induced by excessive ROS production is linked to many processes associated with diabetic cardiovascular complications. Overproduction of ROS resulting from mitochondrial dysfunction or NOX activation is associated with uncoupling of endothelial nitric oxide synthase, which leads to reduced production of nitric oxide and endothelial-dependent vasodilation. Gene silence or inhibitor of NOX reduced oxidized or glycated LDL-induced expression of plasminogen activator inhibitor-1 in endothelial cells. Statins, hypoglycemic agents, and exercise may reduce oxidative stress in diabetic patients through the reduction of NOX activity or the improvement of mitochondrial function, which may prevent or postpone the development of cardiovascular complications.

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