Increased oxidative stress in rats with chronic nitric oxide depletion:measurement of urinary 8-hydroxy-2′-deoxyguanosine excretion

Tsukahara, Hirokazu; Hiraoka, Masahiro; Kobata, Ritsuyo; Hata, Ikue; Ohshima, Yusei; Jiang, Mi Zu; Noiri, Eisei; Mayumi, Mitsufumi

doi:10.1179/rer.2000.5.1.23

Cited by 25 publications

(14 citation statements)

References 25 publications

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“…In this context, previous experimental studies have also shown decreased levels of NOx in obese [34] as well as high-fatfed [35] rats. These findings are consistent with several reports that show the association between chronic NO deficiency induced hypertension and oxidative stress [36] . Plasma NOx levels were significantly increased on GOH supplementation, which may be due to the ability of GOH to induce eNOS.…”

Section: Discussionsupporting

confidence: 94%

Geraniol attenuates oxidative stress by Nrf2 activation in diet-induced experimental atherosclerosis

Jayachandran

Chandrasekaran

Nalini

2014

Journal of Basic and Clinical Physiology and Pharmacology

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Section: Discussionsupporting

confidence: 94%

Geraniol attenuates oxidative stress by Nrf2 activation in diet-induced experimental atherosclerosis

Jayachandran

Chandrasekaran

Nalini

2014

Journal of Basic and Clinical Physiology and Pharmacology

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“…2E) seen under NOS inhibition. Assuming that, under physiological conditions, NO serves to counteract increased oxidative stress produced by O 2 Ϫ (28,29) and NO fluxes exceed those of O 2 Ϫ under these conditions, then as the flux of NO drops due to NOS inhibition, it temporarily passes through the point where its value matches that of O 2 Ϫ , and thus to a level where production of ONOO Ϫ is optimal. This conjecture would account not only for the transient increases in NO-derived products but also for the appar- ent correlation between the amplitude of the nitrate͞nitrite ratios shown in Fig.…”

Section: Discussionmentioning

confidence: 99%

Cellular targets and mechanisms of nitros(yl)ation: An insight into their nature and kinetics in vivo

Bryan

Rassaf²,

Maloney³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

383

343

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There is mounting evidence that the established paradigm of nitric oxide (NO) biochemistry, from formation through NO synthases, over interaction with soluble guanylyl cyclase, to eventual disposal as nitrite͞nitrate, represents only part of a richer chemistry through which NO elicits biological signaling. Additional pathways have been suggested that include interaction of NO-derived metabolites with thiols and metals to form S-nitrosothiols (RSNOs) and metal nitrosyls. Despite the overwhelming attention paid in this regard to RSNOs, little is known about the stability of these species, their significance outside the circulation, and whether other nitros(yl)ation products are of equal importance. We here show that N-nitrosation and heme-nitrosylation are indeed as ubiquitous as S-nitrosation in vivo and that the products of these reactions are constitutively present throughout the organ system. Our study further reveals that all NO-derived products are highly dynamic, have fairly short lifetimes, and are linked to tissue oxygenation and redox state. Experimental evidence further suggests that nitroso formation occurs substantially by means of oxidative nitrosylation rather than NO autoxidation, explaining why S-nitrosation can compete effectively with nitrosylation. Moreover, tissue nitrite can serve as a significant extravascular pool of NO during brief periods of hypoxia, and tissue nitrate͞nitrite ratios can serve as indicators of the balance between local oxidative and nitrosative stress. These findings vastly expand our understanding of the fate of NO in vivo and provide a framework for further exploration of the significance of nitrosative events in redox sensing and signaling. The findings also raise the intriguing possibility that N-nitrosation is directly involved in the modulation of protein function.nitrosothiols ͉ nitrosamines ͉ heme-nitrosyls ͉ ascorbate ͉ oxidative stress T he endogenous production of nitric oxide (NO) by NO synthase (NOS) has been established as playing an important role in vascular homeostasis, neurotransmission, and host defense mechanisms (1). Many of these actions are thought to be mediated by means of stimulation of soluble guanylyl cyclase (sGC) and formation of the second messenger, guanosine 3Ј,5Ј-cyclic monophosphate (cGMP), after which NO is disposed in the form of inactive products, such as nitrite and nitrate. There is mounting evidence, however, that the above scenario represents only part of a broader array of alternative biochemical pathways through which NO can trigger or modulate cell signaling, including interaction with thiols and metals (2). Of those pathways, the best known is the concept of thiol nitrosation, often referred to as ''S-nitrosylation,'' § a posttranslational protein modification that occurs independent of the sGC͞cGMP pathway and could play a critical role in health and disease (3). S-nitroso species (RSNOs) have been implicated in controlling oxygen delivery to tissues, modulating the function or activity of transcription factors, enzymes, memb...

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“…Maximum oxidant production will occur presumably by formation of ONOO -when fluxes of each radical are identical (the flux ratio of each radical is 1.0), especially in regions of low SOD activity. Endothelial activation (as represented by overproduction of O 2 -induced by TNF-α treatment [155][156][157][158]) and dysfunction (as represented by diminished NO synthesis [159][160][161]) might both produce a situation in which a situation of balance of NO and O 2 -in favor of NO is altered in favor of a more oxidative environment.…”

Section: Imbalance Of No/o 2 -Formationmentioning

confidence: 99%

Biomarkers for Oxidative Stress: Clinical Application in Pediatric Medicine

Tsukahara

2007

CMC

118

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Loads of reactive oxygen species (ROS), including superoxide anion and nitric oxide, that overburden antioxidant systems induce oxidative stress in the body. Major cellular targets of ROS are membrane lipids, proteins, nucleic acids, and carbohydrates. Circumstantial evidence suggests that ROS play a crucial role in the initiation and progression of various diseases in children and adolescents. The involvement of ROS and oxidative stress in pediatric diseases is an important concern, but oxidative stress status in young subjects and appropriate methods for its measurement remain to be defined. Recently, specific biomarkers for oxidative damage and antioxidant defense have been introduced into the field of pediatric medicine. This review is intended to provide an overview of clinical applications of oxidative stress biomarkers in the field of pediatric medicine. First, this review presents the biochemistry and pathophysiology of ROS and antioxidant defense systems. Second, it presents a list of clinically applicable biomarkers, along with pediatric diseases in which enhanced oxidative stress might be involved. The discussion emphasizes that several reliable biomarkers are easily measurable using enzyme-linked immunosorbent assay. Third, this review presents age-related reference normal ranges of oxidative stress biomarkers, including urinary acrolein-lysine, 8-hydroxy-2'-deoxyguanosine, nitrite/nitrate, and pentosidine, and the changes of the parameters in several clinical conditions, including atopic dermatitis and diabetes mellitus. New and interesting data on oxidative stress and antioxidant defenses in neonatal biology are also presented. Fourth, this review discusses the ever-accumulating body of data linking oxidative stress to disturbances of the nitric oxide system and vascular endothelial activation/dysfunction. Finally, this review describes the reported clinical trials that have evaluated the efficacy of antioxidants for oxidative-stress related diseases. Suggestions are advanced for the direction of future trials using antioxidant therapies. Repeated measurement of appropriate parameters will enable us to discern the pathophysiological patterns of pediatric diseases and guide our therapies appropriately.

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Increased oxidative stress in rats with chronic nitric oxide depletion:measurement of urinary 8-hydroxy-2′-deoxyguanosine excretion

Cited by 25 publications

References 25 publications

Geraniol attenuates oxidative stress by Nrf2 activation in diet-induced experimental atherosclerosis

Geraniol attenuates oxidative stress by Nrf2 activation in diet-induced experimental atherosclerosis

Cellular targets and mechanisms of nitros(yl)ation: An insight into their nature and kinetics in vivo

Biomarkers for Oxidative Stress: Clinical Application in Pediatric Medicine

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