Nitric oxide as an antioxidant

Kanner, Joseph; Harel, Stella; Granit, Rina

doi:10.1016/0003-9861(91)90452-o

Cited by 417 publications

(198 citation statements)

References 45 publications

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“…In agreement with the hypothesis that NO is part of the system controlling Fe uptake in the first instance of exposure, we showed that NO content in DG was drastically decreased by day 2 of treatment. On the other hand, NO has previously been shown to inhibit lipid peroxidation in many biological systems (Dee et al, 1991;Kanner et al, 1991;Hogg et al, 1993;Rubbo et al, 1994;Gorbunov et al, 1995;Sharpe et al, 2003) through its ability of binding catalytically active Fe (Radi et al, 1995). Thus, the decreased NO content in DG measured by day 2 of exposure to excess Fe could also play a role in the increase in lipid peroxidation, as previously proposed for other biological systems (Radi et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

González

Abele

Puntarulo

2010

Comparative Biochemistry and Physiology Part C: Toxicology &

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The effect of in vivo Fe exposure on the oxidative metabolism of the bivalve Mya arenaria was studied. Fe was supplemented in natural seawater and resulted in a significant increase in the total Fe content in the bivalve digestive gland (DG) between 9 to 17 days of exposure. Mortality of treated animals increased drastically after day 18. Oxidative stress conditions were characterized in DG through assessment of the generation of reactive oxygen species (ROS) and ascorbyl radical (A•) content. Both parameters were affected following a biphasic profile showing significant increases by days 2 and 9 of Fe exposure. The content of 2-thiobarbituric acid reactive substances (TBARS) was significantly increased over control values by days 2, 9 and 17 of treatment. The labile Fe pool (LIP) in isolated DG was elevated over control values by day 7, and maintained this increase until day 17 of Fe exposure. The content of NO, assessed by EPR spin trapping, was 60% lower in DG of animals exposed for 2 days to Fe than in control values, with no further changes. The biphasic profile of oxidative stress response to Fe exposure in DG suggests that at early stages of Fe supplementation the cellular control mechanisms, such as CAT activity, were operative to limit oxidative damage, but further Fe exposure overwhelmed these abilities. Moreover, the second phase could be understood as the consequence of the exhaustion of cellular protective systems that could also involve NO.

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Section: Discussionmentioning

confidence: 99%

Exposure to excess dissolved iron in vivo affects oxidative status in the bivalve Mya arenaria

González

Abele

Puntarulo

2010

Comparative Biochemistry and Physiology Part C: Toxicology &

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“…40 The endothelial damage in diabetic eNOS KO mice may be caused by increased cellular oxidative stress. However, we think this mechanism is less likely.…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Endothelial Nitric-Oxide Synthase Confers Susceptibility to Diabetic Nephropathy in Nephropathy-Resistant Inbred Mice

Kanetsuna

Takahashi

Nagata

et al. 2007

The American Journal of Pathology

165

150

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Recent studies have implicated dysfunctional endothelial nitric-oxide synthase (eNOS) as a common pathogenic pathway in diabetic vascular complications. However, functional consequences are still incompletely understood. To determine the role of eNOS-derived nitric oxide (NO) in diabetic nephropathy, we induced diabetes in eNOS knockout (KO) and wild-type (WT) mice on the C57BL6 background, using low-dose streptozotocin injection, and we investigated their glomerular phenotype at up to 20 weeks of diabetes. Although the severity of hyperglycemia in diabetic eNOS KO mice was similar to diabetic WT mice, diabetic eNOS KO mice developed overt albuminuria, hypertension, and glomerular mesangiolysis, whereas diabetic WT and nondiabetic control mice did not. Glomerular hyperfiltration was also significantly reduced in diabetic eNOS KO mice. Electron micrographs from diabetic eNOS KO mice revealed an injured endothelial morphology, thickened glomerular basement membrane, and focal foot process effacement. Furthermore, the anionic sites at glomeru- Nitric oxide (NO) is a free radical that mediates diverse functions in a range of biological systems.1 NO is produced by a family of nitric-oxide synthase (NOS) enzymes to catalyze the stoichiometric five-electron oxidation of the terminal quanidino group of L-arginine to produce NO and L-citrulline. Three NOS isoforms have been distinguished in mammalian species: neuronal NOS, inducible NOS, which is expressed in a variety of activated tissues, and endothelial NOS (eNOS).1 In the vasculature, NO is mostly generated by eNOS, and the generated NO plays a crucial role in maintaining vascular homeostasis, including vascular tone, leukocyte adhesion to endothelium, proliferation of vascular smooth muscle cells, and platelet aggregation and adhesion to the vessel wall.

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“…NO has been reported to be a free radical scavenger (Kanner et al 1991). For example, the ability of NO to scavenge superoxide anion (O 2 -) has been documented both in vitro (Rubanyi et al 1991) and in vivo ).…”

Section: Anti-oxidant Activitymentioning

confidence: 99%