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Nitric Oxide And Its Role In Health And Diabetes

Role Of Nitric Oxide In The Pathogenesis Of Diabetic Nephropathy In Streptozotocin-induced Diabetic Rats

Role Of Nitric Oxide In The Pathogenesis Of Diabetic Nephropathy In Streptozotocin-induced Diabetic Rats

Role of Nitric Oxide in the Pathogenesis of Diabetic Nephropathy in Streptozotocin-Induced Diabetic Rats Department of Internal Medicine, Chonnam University Medical School, Kwangju, Korea *Department of Physiology, Chonnam University Medical School, Kwangju, Korea Address reprint requests to: Ki Chul Choi, M.D., Ph.D., Department of Internal Medicine, Chonnam University Medical School, 8, Hak-Dong, Dong-Ku, Kwangju, 501-757, Korea Author information Copyright and License information Disclaimer Copyright 1999 The Korean Association of Internal Medicine This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( ) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Several reports suggest that enhanced generation or actions of nitric oxide (NO) have been implicated in the pathogenesis of glomerular hyperfiltration and hyperperfusion that occurs in early diabetes. However, the precise role of altered NO generation in the pathogenesis of diabetic nephropathy is unclear. The present study was aimed at investigating the role of nitric oxide in the pathogenesis of glomerular hyperfiltration and hyperperfusion in streptozotocin-induced diabetic rats. To evaluate the role of NO in diabetic hyperfiltration, we measured plasma and urine concentrations of NO2/NO3, stable metabolic products of NO and protein expressions of three isoforms of nitric oxide synthase (NOS) in streptozotocin-induced diabetic rats. We also investigated renal hemodynamic changes, such as glomerular filtration rate (GFR) and renal plasma flow (RPF), in responses to acute and chronic administration of NO synthes Continue reading >>

Role Of Nitric Oxide Synthase Family In Diabetic Neuropathy

Role Of Nitric Oxide Synthase Family In Diabetic Neuropathy

Type 1 diabetes; Type 2 diabetes; Diabetic neuropathy; Nitric oxide system; NOS gene polymorphisms T1DM: Type 1 Diabetes; T2DM: Type 2 Diabetes; DN: Diabetic Neuropathy; DPN: Diabetic Polyneuropathy; DSPN: symmetrical, length-dependent Diabetic Sensorimotor Poly Neuropathy; DAN: Diabetic Autonomic Neuropathy; ROS: Reactive Oxygen Species; PARP: Poly ADP-Ribose Polymerase; PKC: Protein Kinase C; AGE: Advanced Glycation End-products; AKR1B1: Aldose Reductase Gene; GWL: Genome Wide Scan Linkage; GWA: Genome Wide Scan Association; NO: Nitric Oxide; RBC: Red Blood Cells; NOx: Stable end-product Nitrite/Nitrate; NOS1: Neuronal Nitric Oxide Synthase; NOS2: Inducible Nitric Oxide Synthase; NOS3: Endothelial Nitric Oxide Synthase; SNP: Single Nucleotide Polymorphism; rs1799983: The G to T polymorphism at position 894 in exon 7 of NOS3 gene; rs2070744: The substitution from T to C at the position -786 in the promoter region of NOS3 gene. Diabetes mellitus is one of the most prevalent chronic diseases of modern societies and a major health problem in nearly all countries. Its prevalence has risen sharply worldwide during the past few decades [ 1 ]. Moreover, predictions for the next 20 years show that diabetes prevalence will continue to rise, reaching epidemic proportions by 2030: 439 million adults worldwide representing 7.7% of the total world population [ 1 ]. This increase in the prevalence is largely due to the epidemic of obesity and consequent type 2 diabetes (T2DM), but type 1 diabetes (T1DM) incidence is also rising in all developing countries [ 2 ]. Both T1DM and T2DM are characterized by the slow progression towards the generation of some specific lesions of the blood vessels affecting both small (microangiopathy) and larger (macroangiopathy) vessels. The classical mi Continue reading >>

Microvascular Oxidative Stress In The Triad Of Cardiovascular, Metabolic And Renal Disease

Microvascular Oxidative Stress In The Triad Of Cardiovascular, Metabolic And Renal Disease

Department of Physiology and Pharmacology Cardiovascular disease and diabetes are increasing health problems worldwide, resulting in an enormous economic burden to society. To better understand, prevent and cure these lifestyle diseases it is necessary to research the underlying mechanisms that allow the diseases to arise. The kidneys set the long-term level of blood pressure by regulating peripheral vascular resistance and body fluid volume. It is suggested that impaired renal function importantly contributes to the development of hypertension, which is a main risk factor for morbidity and mortality complications from cardiovascular diseases and type 2 diabetes. Moreover, renal dysfunction is commonly described as a complication of metabolic syndrome, but new knowledge shows that renal disease actually may antecede the syndrome. Approximately 25 per cent of the worlds adult population has the metabolic syndrome (cluster of obesity, dyslipidemia, hyperglycemia, and hypertension). These individuals are at a higher risk of developing cardiovascular disease and type 2 diabetes. Renal oxidative stress and nitric oxide in cardiovascular disease and diabetes Emerging evidence suggests that renal oxidative stress and nitric oxide deficiency is associated with cardiovascular disease and diabetic complications. Currently the mechanisms are not clear, but imbalance between reactive oxygen species and nitric oxide (in favour of the former) may impair renal autoregulatory function, and thus impact on renal blood flow and glomerular filtration. Using a translational approach (in vitro and in vivo microperfusion systems, genetically modified mice, and clinical trials) our projects aim to further characterize mechanisms for reactive oxygen species and nitric oxide formation, interac Continue reading >>

Characterization Of The Role Of Nitric Oxide And Its Clinical Applications

Characterization Of The Role Of Nitric Oxide And Its Clinical Applications

Characterization of the Role of Nitric Oxide and Its Clinical Applications Levine A.B.a Punihaole D.b Levine T.B.a Nitric oxide (NO) has long been known as endothelium-derived relaxing factor. It is a vasodilator, modulating vascular tone, blood pressure and hemodynamics, a role exploited by nitrate donor therapy for angina, heart failure, pulmonary hypertension and erectile dysfunction. In addition, its powerful antioxidant, anti-inflammatory and antithrombotic actions are antiatherogenic with antiatherothrombotic impact. NO signaling modulates skeletal muscle and myocardial contractility and metabolism and is intimately linked with insulin signaling. Vascular and muscle NO signaling coordinate skeletal muscle and myocardial energy demand with supply and are critical for both carbohydrate and fatty acid total-body homeostasis. NO signaling in mitochondria underlies much of NOs metabolic effect, which, at low physiologic levels, links cellular energy demand with mitochondrial energy supply, while beneficially affecting mitochondrial oxidative stress and calcium handling. Mitochondria are also the site for the life-threatening deleterious effects arising from inflammation-related excessive NO levels. NO-deficient states are characterized by cell senescence, oxidative stress, inflammation, endothelial dysfunction, vascular disease, insulin resistance and type 2 diabetes mellitus. NO-enriching therapy would be expected to be of benefit not only for its hemodynamic but also for its metabolic impact. In contrast, strategies are needed to curtail excessive NO in states such as septic shock. Nitric oxide (NO) is best known for its actions in the vasculature. In addition, NO plays a key role in cell metabolism and is instrumental in coordinating tissue energy demand with suppl Continue reading >>

Diabetic Endothelial Nitric Oxide Synthase Knockout Mice Develop Advanced Diabetic Nephropathy

Diabetic Endothelial Nitric Oxide Synthase Knockout Mice Develop Advanced Diabetic Nephropathy

Diabetic Endothelial Nitric Oxide Synthase Knockout Mice Develop Advanced Diabetic Nephropathy *Division of Nephrology, Molecular Pathology and Immunology Core Lab, and Department of Pathology, Immunology and Laboratory Medicine, University of Florida, and Pathology and Laboratory Medicine Service, North Florida/South Georgia Veterans Health System, Gainesville Florida; and Department of Clinical Immunology of Internal Medicine, Nagoya University Graduate School of Medicine, Nagoya, Japan Dr. Takahiko Nakagawa, Division of Nephrology, Hypertension and Transplantation, University of Florida, PO Box 100224, Gainesville, FL 32610-0224. Phone: 352-392-2448; Fax: 352-392-5465; E-mail; nakagt{at}medicine.ufl.edu Accepted for publication October 31, 2006. The pathogenesis of diabetic nephropathy remains poorly defined, and animal models that represent the human disease have been lacking. It was demonstrated recently that the severe endothelial dysfunction that accompanies a diabetic state may cause an uncoupling of the vascular endothelial growth factor (VEGF)-endothelial nitric oxide (eNO) axis, resulting in increased levels of VEGF and excessive endothelial cell proliferation. It was hypothesized further that VEGF-NO uncoupling could be a major contributory mechanism that leads to diabetic vasculopathy. For testing of this hypothesis, diabetes was induced in eNO synthase knockout mice (eNOS KO) and C57BL6 controls. Diabetic eNOS KO mice developed hypertension, albuminuria, and renal insufficiency with arteriolar hyalinosis, mesangial matrix expansion, mesangiolysis with microaneurysms, and Kimmelstiel-Wilson nodules. Glomerular and peritubular capillaries were increased with endothelial proliferation and VEGF expression. Diabetic eNOS KO mice showed increased mortality at 5 Continue reading >>

Hyperglycaemia Enhances Nitric Oxide Production In Diabetes: A Study From South Indian Patients

Hyperglycaemia Enhances Nitric Oxide Production In Diabetes: A Study From South Indian Patients

Hyperglycaemia Enhances Nitric Oxide Production in Diabetes: A Study from South Indian Patients Affiliation Division of Medicinal Chemistry and Pharmacology, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Biomaterials Group, Lipid Science and Technology Division, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Division of Medicinal Chemistry and Pharmacology, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Biomaterials Group, Lipid Science and Technology Division, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Division of Medicinal Chemistry and Pharmacology, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Division of Medicinal Chemistry and Pharmacology, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Biomaterials Group, Lipid Science and Technology Division, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Affiliation Cardiology Division, Mediciti Hospital, Hyderabad, 500063, India Current Address: Drug Discovery Research Center, Translational Health Science and Technology Institute (THSTI), Faridabad, 121001, India Affiliation Division of Medicinal Chemistry and Pharmacology, Indian Institute of Chemical Technology (CSIR-IICT), Hyderabad, 500007, India Continue reading >>

Nitric Oxide And Diabetes

Nitric Oxide And Diabetes

Scientists around the world are working feverishly to increase our understanding of the nitric oxide in the human body. The results so far have been nothing short of astounding. Having already identified numerous incredible benefits related to increased blood, oxygen and nutrient flow, scientists are now doing research into the effect of nitric oxide on some of society’s most vexing health issues like diabetes. Diabetics have a lower level of nitric oxide than normal and that low NO may contribute to the complications that plague diabetics. Nitric oxide may ameliorate the symptoms of of the associated conditions inherent to diabetes like reduced blood flow, kidney disease, retinopathy and ulcers. The effect of nitric oxide on diabetes is a very important topic for personal reasons. My oldest son was diagnosed with Type 1 diabetes at age 7. As opposed to Type 2 diabetes which is characterized by insulin resistance, in Type 1 Diabetes, the body produces too little or no insulin at all. Insulin is a critical hormone for causing the cells to take up glucose, their primary fuel. Without insulin, there is no way for the glucose to get into the cells. Without glucose, the cells die. Perhaps out of desperation, when the body notices a lack of insulin, it starts to burn fats. That may sound great to some people, but it can be devastating. Your internal organs and brain are mostly made of fats and become a food source in this desperate situation. Without insulin, no matter what the body breaks apart to use for fuel, it cannot get glucose into the cells. However, the glucose, or sugar doesn’t just go away, it stays in the blood. The body does try to excrete the excess glucose through the urine, however, it ends up becoming dehydrated because of the reverse osmosis that pulls w Continue reading >>

Nitric Oxide - Diabetes Self-management

Nitric Oxide - Diabetes Self-management

A clear, colorless gas that performs a number of important functions in the body. It seems to play a role in several medical conditions, including septic shock, dementia, and impotence, and it may partially account for the high rate of heart disease seen in people with diabetes. Nitric oxide is considered such an important chemical in the body that the journal Science named it the Molecule of the Year in 1992, and in 1998 three scientists won the Nobel Prize in Medicine for researching its role in the body. Scientists have long been familiar with nitric oxide as a component of car exhaust, cigarette smoke, and air pollution, but it wasnt until the late 1980s that researchers discovered that mammal cells also produce the gas and use it to communicate with other cells. Abnormalities in the bodys production of nitric oxide have been implicated in high blood pressure, atherosclerosis (narrowing of the arteries), diabetes, erectile dysfunction, and stroke. Scientists are furthest along in their understanding of nitric oxide in the area of heart disease. Normally, cells lining the inner wall of blood vessels secrete nitric oxide, which travels to the muscle cells around the blood vessels and causes them to widen, allowing easier blood flow. Impaired nitric oxide production may contribute to constricted blood vessels, high blood pressure (especially in the 90% of cases with no identifiable cause), and atherosclerosis. Scientists now know that nitroglycerin and similar drugs dilate blood vessels and help alleviate angina temporary chest pain resulting from insufficient oxygen to the heart because the drugs release nitric oxide. Nitric oxide also keeps blood platelets from clumping together and sticking to the inner walls of arteries, protecting the body from blood clots and at Continue reading >>

Paradoxes Of Nitric Oxide In The Diabetic Kidney

Paradoxes Of Nitric Oxide In The Diabetic Kidney

Paradoxes of nitric oxide in the diabetic kidney Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, and Diabetes Center, Institute of Clinical and Experimental Medicine, Prague, Czech Republic Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, and Portland Veterans Affairs Medical Center, Portland, Oregon 97201-2940; and As an important modulator of renal function and morphology, the nitric oxide (NO) system has been extensively studied in the diabetic kidney. However, a number of studies in different experimental and clinical settings have produced often confusing data and contradictory findings. We have reviewed a wide spectrum of findings and issues that have amassed concerning the pathophysiology of the renal NO system in diabetes, pointed out the controversies, and attempted to find some explanation for these discrepancies. Severe diabetes with profound insulinopenia can be viewed as a state of generalized NO deficiency, including in the kidney. However, we have focused our hypotheses and conclusions on the events occurring during moderate glycemic control with some degree of treatment with exogenous insulin, representing more the clinically applicable state of diabetic nephropathy. Available evidence suggests that diabetes triggers mechanisms that in parallel enhance and suppress NO bioavailability in the kidney. We hypothesize that during the early phases of nephropathy, the balance between these two opposing forces is shifted toward NO. This plays a role in the development of characteristic hemodynamic changes and may contribute to consequent structural alterations in glomeruli. Both endothelial (eNOS) and neuronal NO synthase can contribute to altered NO pro Continue reading >>

Frontiers | The Role Of Nitric Oxide In The Dysregulation Of The Urine Concentration Mechanism In Diabetes Mellitus | Physiology

Frontiers | The Role Of Nitric Oxide In The Dysregulation Of The Urine Concentration Mechanism In Diabetes Mellitus | Physiology

Front. Physiol., 06 June 2012 | The role of nitric oxide in the dysregulation of the urine concentration mechanism in diabetes mellitus Penelope Cipriani, Sunhye L. Kim , Janet D. Klein , Jae H. Sim, Tobias N. von Bergen and Mitsi A. Blount * Renal Division, Department of Medicine, Emory University, Atlanta, GA, USA Uncontrolled diabetes mellitus results in osmotic diuresis. Diabetic patients have lowered nitric oxide (NO) which may exacerbate polyuria. We examined how lack of NO affects the transporters involved in urine concentration in diabetic animals. Diabetes was induced in rats by streptozotocin. Control and diabetic rats were given L-NAME for 3 weeks. Urine osmolality, urine output, and expression of urea and water transporters and the Na-K-2Cl cotransporter were examined. Predictably, diabetic rats presented with polyuria (increased urine volume and decreased urine osmolality). Although metabolic parameters of control rats were unaffected by L-NAME, treated diabetic rats produced 30% less urine and osmolality was restored. UT-A1 and UT-A3 were significantly increased in diabetic rat inner medulla. While L-NAME treatment alone did not alter UT-A1 or UT-A3 abundance, absence of NO prevented the upregulation of both transporters in diabetic rats. Similarly, AQP2 and NKCC2 abundance was increased in diabetic animals however, expression of these transporters were unchanged by L-NAME treatment of diabetes. Increased expression of the concentrating transporters observed in diabetic rats provides a compensatory mechanism to decrease solute loss despite persistent glycosuria. Our studies found that although diabetic-induced glycosylation remained increased, total protein expression was decreased to control levels in diabetic rats treated with L-NAME. While the role of Continue reading >>

Role Of Nitric Oxide In Insulin-dependent Diabetes Mellitus-related Vascular Complications.

Role Of Nitric Oxide In Insulin-dependent Diabetes Mellitus-related Vascular Complications.

Role of nitric oxide in insulin-dependent diabetes mellitus-related vascular complications. This article has been cited by other articles in PMC. Patients with insulin-dependent diabetes mellitus are at high risk for vascular disorders such as hypertension, nephropathy, and retinopathy. The most common cause of morbidity and mortality in patients with insulin-dependent diabetes is vascular disease. Despite ongoing research, the pathogenesis of vascular disease in diabetes remains unclear. In recent years, numerous investigators have examined the role of the endothelium-derived relaxing factor, nitric oxide, in the disease state of hypertension and its complications. We review the role of nitric oxide in the development of diabetes-related vascular disease and discuss findings suggesting that nitric oxide metabolism and vascular responsiveness to nitric oxide are altered in diabetes. Patients with diabetes may benefit from therapy that addresses this pathogenic deficiency. Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.6M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . Click on the image to see a larger version. These references are in PubMed. This may not be the complete list of references from this article. Furchgott RF. Introduction to EDRF research. J Cardiovasc Pharmacol. 1993;22 (Suppl 7):S1S2. [ PubMed ] Moncada S, Palmer RM, Higgs EA. Nitric oxide: physiology, pathophysiology, and pharmacology. Pharmacol Rev. 1991 Jun;43(2):109142. [ PubMed ] Lowenstein CJ, Dinerman JL, Snyder SH. Nitric oxide: a physiologic messenger. Ann Intern Med. 1994 Feb 1;120(3):227237. [ PubMed ] Anderson J, Rocchini AP. Hypertension in Continue reading >>

Using Nitric Oxide To Help Treat Diabetes

Using Nitric Oxide To Help Treat Diabetes

We're sorry, an error occurred. We are unable to collect your feedback at this time. However, your feedback is important to us. Please try again later. Further to my query on natural substances that help diabetes, have you heard of Nitric Oxide (NO)? Sounds toxic, ay? It is in fact a "free radical gas that is a powerful regulator of circulation (it is an endogenous vasodilator) and a neurotransmitter (it helps in the processing of nerve signals as they cross synapses)." Read all about it at DiabetesInControl . Apparently NO is impaired in people with both Type 1 and Type 2 diabetes, and this deficiency may play an important role in the poor circulation in diabetic patients that leads to high incidence of ulcers. Some researchers also believe the NO shortage is one cause of peripheral neuropathy (diabetic nerve damage). In short, impaired circulation is indeed the root of most diabetic complicaitons, and NO seems to have a powerful effect in improving this problem. So where can I get me some NO?! The January issue of the medical journal Diabetes features a paper by several doctors proposing NO as a potential new diabetes treatment. The authors experimented with adding "physiologic concentrations" of NO to the CD34+cells, which repair blood vessels throughout the body -- working with cells taken from diabetic patients in a lab setting. According to the experts, this work takes "groundbreaking" strides towards halting diabetic complications. We're talking fully regenerated cell repair . Too late for my father, but here's an advancement that Our D-Generation might actually benefit from. Disclaimer: Content created by the Diabetes Mine team. For more details click here. This content is created for Diabetes Mine, a consumer health blog focused on the diabetes community. The Continue reading >>

Nitric Oxide Holds Promise For Diabetes Cell Repair

Nitric Oxide Holds Promise For Diabetes Cell Repair

University of Florida researchers say primitive cells that act like molecular maintenance men—traveling throughout the body to repair damaged blood vessels—become too rigid in patients with diabetes, fueling the disease’s vascular complications. But they have found a way to restore the cells’ flexibility, at least in the laboratory, according to findings published in the January 2006 issue of the journal Diabetes. Many complications of diabetes, such as heart disease, stroke, blindness, and kidney failure, arise after blood vessels suffer damage, spurring the accumulation of fatty deposits in the arteries, or an overgrowth of new capillaries in the eye. “We’re interested in what happens in the body at the molecular level to cause these life-threatening problems,” says Mark S. Segal, PhD, an assistant professor of nephrology, hypertension, and transplantation at UF’s College of Medicine. “Our work is focused on understanding why diabetic patients are at increased risk for these other diseases.” CELLS FAIL TO REPAIR The problem is rooted in the body’s response to vascular injury. The bone marrow churns out cells crucial to repairing the damaged lining of blood vessels. But sometimes these cells fail to report for duty. “Part of the defect we think is occurring in diabetic patients is that these cells do not carry out appropriate repair,” Segal said. The inability of these cells to repair the large blood vessels of the body is similar to their inability to repair the small vessels within the eye, he added. “In the vasculature, it leads to atherosclerosis, and within the eye, the same process leads to diabetic retinopathy,” he said. “So the link is we have one defect in these cells that can lead to both of these problems.” NITRIC OXIDE IS K Continue reading >>

Increased Plasma Concentration Of Nitric Oxide In Type 2 Diabetes But Not In Nondiabetic Individuals With Insulin Resistance - Em|consulte

Increased Plasma Concentration Of Nitric Oxide In Type 2 Diabetes But Not In Nondiabetic Individuals With Insulin Resistance - Em|consulte

Doi : DM-02-2005-31-1-1262-3636-101019-200512010 Increased plasma concentration of nitric oxide in type 2 diabetes but not in nondiabetic individuals with insulin resistance WY Chien[1], KD Yang[2], HL Eng[3], YH Hu[1], PY Lee[4], ST Wang[5], PW Wang[1] [1]Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung [2]Pediatrics, Chang Gung Memorial Hospital, Kaohsiung [3]Pathology, Chang Gung Memorial Hospital, Kaohsiung [4]Pharmacy, Chang Gung Memorial Hospital, Kaohsiung [5]Department of Public Health, National Cheng Kung University Medical Center, Tainan, Taiwan. [1]Chang Gung Memorial Hospital, 123, Ta-Pei Road, Niao-Sung Hsiang, Kaohsiung Hsien, Taiwan. Augmentation des concentrations plasmatiques de monoxyde d'azote chez le diabtique de type 2, mais non chez le sujet non diabtique insulino-rsistant L'insulino-rsistance (IR) est un lment cl de la pathognie du diabte de type 2. Les rsultats d'exprimentations rcentes sur la vasodilatation mdie par l'insuline ont suggr que l'insensibilit vasculaire est un composant de l'IR. Cependant, la notion d'une rduction de la capacit de l'insuline augmenter la libration endothliale de monoxyde d'azote (NO) chez le diabtique de type 2 est controverse. Les concentrations plasmatiques de NO ont t determines chez 26 diabtiques de type 2 et 78 volontaires non diabtiques lors d'un test de suppression insulinique. Le test mesure l'efficacit de l'insuline promouvoir l'utilisation d'une charge en glucose perfuse, la glycmie en tat stable (steady state plasma glucose SSPG) au cours des 150-180min du test tant choisie comme index d'IR. Les concentrations plasmatiques de NO ont t dtermines par mesure des produits finaux stables de son mtabolisme. La comparaison des concentrations plasmatiques de NO entre les groupes a t effec Continue reading >>

Nitric Oxide And Its Role In Lipid Peroxidation

Nitric Oxide And Its Role In Lipid Peroxidation

Istituto di I Clinica Medica, University La Sapienza, Rome, Italy Istituto di I Clinica Medica, University La Sapienza, Rome, Italy Please review our Terms and Conditions of Use and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Use the link below to share a full-text version of this article with your friends and colleagues. Learn more. Nitric oxide (NO) is a free radical with an unpaired electron in the highest orbital. This is why it behaves as a potential antioxidant agent by virtue of its ability to reduce other molecules. In vitro experiments support this concept inasmuch as NO is able to inhibit lipid peroxidation. However, NO is rapidly inactivated by the superoxide anion (O ) to form peroxynitrite (ONOO), which is a potent oxidant. Therefore, in the presence of O , NO behaves as a potent prooxidant. This is the mechanism that accounts for the low density lipoprotein (LDL) oxidation that occurs when NO and O are simultaneously present in the medium. As NO and O are simultaneously released by cells such as endothelial cells, the balance between these two radicals is crucial in understanding the net effect of NO on lipid peroxidation. Thus an excess of NO will favour lipid peroxidation inhibition, while an excess of O will induce lipid peroxidation. Modulation of this balance may have important clinical implications, particularly in the atherosclerotic process in which oxidant stress seems to play a pivotal role in the onset and progression of vascular lesions. Copyright 1999 John Wiley & Sons, Ltd. Nitric oxide (NO) is a ubiquitous molecule which is formed intracellularly by Larginine metabolism. It is a highly reactive molecule because it contains an unpaired electron in the hig Continue reading >>

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