Reactive Oxygen and Nitrogen Species

Salisbury, Dereck; Bronas, Ulf G.

doi:10.1097/nnr.0000000000000068

Cited by 111 publications

(55 citation statements)

References 82 publications

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“…In addition to Zn 2+ , GSNOR also requires a coenzyme that can vary based upon the substrate. These include: nicotinamide adenine dinucleotide (NAD+), its reduced form NADH, NADPH + H + , or NAD(P)+ (Gupta, Kapuganti Jagadis, 2015; Hedberg et al, 2003; Jensen et al, 1998; Sanghani et al, 2000). …”

Section: Adh5: Structure/localizationmentioning

confidence: 99%

“…HMGSH binds at the zinc active site and interacts with the highly conserved residues Arg114/115, Asp55, Glu57, and Thr46 (Engeland et al, 1993; Sanghani et al, 2002). That being said, the rate of substrate conversion (K cat ) is about 20-fold higher for GSNO over HMGSH (Green et al, 2012; Hedberg et al, 2003; Salisbury and Bronas, 2015; Sanghani et al, 2000; Claudia A Staab et al, 2008). Both reactions are dependent on an abundant source glutathione (GSH) in the cell.…”

Section: Substratesmentioning

confidence: 99%

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The role of S-nitrosoglutathione reductase (GSNOR) in human disease and therapy

Barnett

Buxton

2017

Critical Reviews in Biochemistry and Molecular Biology

112

101

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S-nitrosoglutathione reductase (GSNOR), or ADH5, is an enzyme in the alcohol dehydrogenase (ADH) family. It is unique when compared to other ADH enzymes in that primary short-chain alcohols are not its principle substrate. GSNOR metabolizes S-nitrosoglutathione (GSNO), S-hydroxymethylglutathione (the spontaneous adduct of formaldehyde and glutathione), and some alcohols. GSNOR modulates reactive nitric oxide (•NO) availability in the cell by catalyzing the breakdown of GSNO, and indirectly regulates S-nitrosothiols (RSNOs) through GSNO-mediated protein S-nitrosation. The dysregulation of GSNOR can significantly alter cellular homeostasis, leading to disease. GSNOR plays an important regulatory role in smooth muscle relaxation, immune function, inflammation, neuronal development, and cancer progression, among many other processes. In recent years, the therapeutic inhibition of GSNOR has been investigated to treat asthma, cystic fibrosis and interstitial lung disease (ILD). The direct action of •NO on cellular pathways, as well as the important regulatory role of protein S-nitrosation, are closely tied to GSNOR regulation and define this enzyme as an important therapeutic target.

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Section: Adh5: Structure/localizationmentioning

confidence: 99%

Section: Substratesmentioning

confidence: 99%

The role of S-nitrosoglutathione reductase (GSNOR) in human disease and therapy

Barnett

Buxton

2017

Critical Reviews in Biochemistry and Molecular Biology

112

101

View full text Add to dashboard Cite

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“…Unfortunately, interventions with folate to reduce homocysteine levels have thus far been conflicting and disappointing [95–97]. Patients with CKD have increased levels of oxidative stress, caused by uremia, production of reactive oxygen species via physiological pathways (e.g., impaired/damaged/malfunctioning mitochondria), and an inability to produce adequate antioxidative enzymes [98, 99]. These changes all contribute to a vascular milieu that consists of systemic inflammation, high levels of oxidative stress, and endothelial dysfunction that is unique to the CKD patient and creates a vascular pathway to cognitive decline.…”

Section: The Cerebrovascular-renal Axis (Figure 1)mentioning

confidence: 99%

Cognitive Impairment in Chronic Kidney Disease: Vascular Milieu and the Potential Therapeutic Role of Exercise

Bronas

Puzantian

Hannan

2017

BioMed Research International

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Chronic kidney disease (CKD) is considered a model of accelerated aging. More specifically, CKD leads to reduced physical functioning and increased frailty, increased vascular dysfunction, vascular calcification and arterial stiffness, high levels of systemic inflammation, and oxidative stress, as well as increased cognitive impairment. Increasing evidence suggests that the cognitive impairment associated with CKD may be related to cerebral small vessel disease and overall impairment in white matter integrity. The triad of poor physical function, vascular dysfunction, and cognitive impairment places patients living with CKD at an increased risk for loss of independence, poor health-related quality of life, morbidity, and mortality. The purpose of this review is to discuss the available evidence of cerebrovascular-renal axis and its interconnection with early and accelerated cognitive impairment in patients with CKD and the plausible role of exercise as a therapeutic modality. Understanding the cerebrovascular-renal axis pathophysiological link and its interconnection with physical function is important for clinicians in order to minimize the risk of loss of independence and improve quality of life in patients with CKD.

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“…ONOO − oxidizes DNA, proteins, lipids, and BH4, uncouples eNOS and limits NO production. ONOO − directly influences the dilatory capabilities of the arteries and disrupts NO-induced sGC-mediated signal transduction [107]. Nevertheless, NO could be transported by protein carriers or stored locally and cause remote and long-lasting effects in the cardiovascular system [108,109].…”

Section: Oxidative Stress and Injurymentioning

confidence: 99%

Vitamin D in Oxidative Stress and Diseases

Uberti¹,

Morsanuto²,

Molinari³

2017

A Critical Evaluation of Vitamin D - Basic Overview

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The data described in this chapter consider some new information about the benefits of vitamin D 3 comparing the results obtained by the authors on the effects of vitamin D 3 during oxidative stress with other works available in the literature. In particular, vitamin D 3 can induce a concentration-dependent increase in endothelial NO production through eNOS activation consequential to the phosphorylation of p38, AKT, and ERK. Additional information obtained by the author is about the ability of vitamin D 3 to prevent the endothelial cell death through modulation of interplay between apoptosis and autophagy. This effect is obtained by inhibiting superoxide anion generation, maintaining mitochondria function and cell viability, activating survival kinases (ERK and Akt), and inducing NO production. The results also describe that vitamin D 3 causes human endothelial cell proliferation and migration in a 3-D matrix through NOdependent mechanisms. These findings support the role of vitamin D 3 in the human angiogenic process, suggesting new applications for vitamin D 3 in tissue repair and wound healing. Finally, that the authors have demonstrated the ability of vitamin D 3 to counteract negative effects of oxidative stress in brain cells. These data suggest the potential therapeutic use of vitamin D to treat or prevent degenerative brain diseases.

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Reactive Oxygen and Nitrogen Species

Abstract: The success and failures of current therapies to reduce oxidative stress are discussed in terms of implications for nursing research on exogenous antioxidants, pharmacotherapy, and lifestyle change.

Cited by 111 publications

References 82 publications

The role of S-nitrosoglutathione reductase (GSNOR) in human disease and therapy

The role of S-nitrosoglutathione reductase (GSNOR) in human disease and therapy

Cognitive Impairment in Chronic Kidney Disease: Vascular Milieu and the Potential Therapeutic Role of Exercise

Vitamin D in Oxidative Stress and Diseases

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