Fenoldopam and <i>N</i>‐acetylcysteine for the Prevention of Radiographic Contrast Material—Induced Nephropathy: A Review

Walker, Paul D.; Brokering, Kristi L.; Theobald, John C.

doi:10.1592/phco.23.15.1617.31958

Cited by 17 publications

(6 citation statements)

References 27 publications

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“…In these trials, N-acetylcysteine was given in addition to the general hydration protocols and showed a positive outcome in four of the studies [44,45,47,49] and has therefore been recommended for the prevention of CIN in patients with mild-to-moderate renal insufficiency [50][51][52]. However, this recommendation is not unequivocal since other trials fail to confirm a positive effect [48,53] or indicate that rigorously controlled larger trials are still required [54].…”

Section: Altered Mitochondrial Function In a Proximal Tubular Cell mentioning

confidence: 99%

Pathophysiology of contrast medium–induced nephropathy

Persson

Hansell

Liss

2005

Kidney International

486

371

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Section: Altered Mitochondrial Function In a Proximal Tubular Cell mentioning

confidence: 99%

Pathophysiology of contrast medium–induced nephropathy

Persson

Hansell

Liss

2005

Kidney International

486

371

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“…Its clinical uses range from mucolytic therapy for patients with inspissated respiratory secretions to standard treatment of acetaminophen overdoses (21). Recently, NAC has also been used for the prevention of contrast-induced nephropathy (22,23). The efficacy of NAC may be secondary to detoxification of OFR, local vasoactive properties, or interference with gene expression (16,20).…”

Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine Improves the Hemodynamics and Oxidative Stress in Hypoxic Newborn Pigs Reoxygenated With 100% Oxygen

Bigam²,

Emara³

et al. 2007

Shock

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Neonatal asphyxia may lead to cardiac and renal complications perhaps mediated by oxygen free radicals. Using a model of neonatal hypoxia-reoxygenation, we tested the hypothesis that N-acetylcysteine (NAC) would improve cardiac function and renal blood flow. Eighteen piglets (aged 1-4 days old, weighing 1.4-2.2 kg) were anesthetized and acutely instrumented for continuous monitoring of pulmonary and renal artery flow (cardiac index [CI] and renal artery flow index [RAFI], respectively) and mean blood pressure. Alveolar hypoxia was induced for 2 h, followed by resuscitation with 100% oxygen for 1 h and 21% oxygen for 3 h. Animals were randomized to sham-operated, hypoxic control, and NAC treatment (i.v. bolus of 150 mg/kg given at 10 min of reoxygenation followed by 100 mg/kg per h infusion) groups. Myocardial and renal tissue glutathione content and lipid hydroperoxide levels were assayed, and histology was examined. After 2 h of hypoxia, all animals were acidotic (pH 6.96 +/- 0.04) and in cardiogenic shock with depressed renal blood flow. Upon reoxygenation, CI and RAFI increased but gradually deteriorated later. The NAC treatment prevented the decreased CI, stroke volume, mean blood pressure, systemic oxygen delivery, RAFI, and renal oxygen delivery at 2 to 4 h of reoxygenation observed in hypoxic controls (versus shams, all P< 0.05). The myocardial and renal tissue glutathione content was significantly higher in the NAC treatment group (versus controls). The CI and RAFI at 4 h of reoxygenation correlated with the tissue glutathione redox ratio (r = 0.5 and 0.6, respectively, P < 0.05). There were no significant differences in heart rate, pulmonary artery pressure, systemic oxygen uptake, and tissue lipid hydroperoxide levels between groups. No histologic injury was found in the heart or kidney. In this porcine model of neonatal hypoxia and 100% reoxygenation, NAC improved cardiac function and renal perfusion, with improved tissue glutathione content.

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“…NAC is a well known amino thiol molecule with clinical uses ranging from mucolytic therapy for patients with inspissated respiratory secretions to standard treatment of acetaminophen overdoses 13) and more recently for the prevention of contrast-induced nephropathy. 14) NAC partly acts as a free radical scavenger as well as a GSH precursor to increase intracellular antioxidant capacity and hence protect cells against ROS. 15) However, it is also thought to work through other mechanisms.…”

mentioning

confidence: 99%

Sulphur Antioxidants Inhibit Oxidative Stress Induced Retinal Ganglion Cell Death by Scavenging Reactive Oxygen Species but Influence Nuclear Factor (Erythroid-Derived 2)-Like 2 Signalling Pathway Differently

Majid

Yin

2013

Biological & Pharmaceutical Bulletin

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This study aimed to show if two different sulphur containing drugs sulbutiamine and acetylcysteine (NAC) could attenuate the effects of two different insults being serum deprivation and glutamate/buthionine sulfoximine (GB)-induced death to transformed retinal ganglion cell line (RGC-5) in culture. Cells were exposed to either 5 mm of GB for 24 h or serum deprivation for 48 h with inclusion of either NAC or sulbutiamine. Cell viability, microscopic evidence for apoptosis, caspase 3 activity, reactive oxygen species (ROS), glutathione (GSH), catalase and gluthathione-S-transferase (GST) were determined. The effects of NAC and sulbutiamine on the oxidative stress related transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf-2) levels and its dependent phase II enzyme haemeoxygenase-1 (HO-1) were carried out using Western blot and quantitative-polymerase chain reaction (PCR). NAC and sulbutiamine dose-dependently attenuated serum deprivation-induced cell death. However NAC but not sulbutiamine attenuated GB-induced cell death. NAC and sulbutiamine both independently stimulated the GSH and GST production but scavenged different types of ROS with different efficacy. Moreover only sulbutiamine stimulated catalase and significantly increased Nrf-2 and HO-1 levels. In addition, the pan caspase inhibitor, benzoylcarbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk) attenuated the negative effect of serum deprivation while the necroptosis inhibitor (necrostatin-1) counteracted solely an insult of GB. The neuroprotective actions of NAC and sulbutiamine in GB or serum-deprivation insult are therefore different.Key words sulphur-antioxidant; oxidative stress; reactive oxygen species; retinal ganglion cell In a neurodegenerative disease like glaucoma, oxidative stress caused by reactive oxygen species (ROS) overproduction is thought to play an important role in causing retinal ganglion cells (RGCs) death.1) ROS over production also appears to play an important role in the pathogenesis of other progressive neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and acute syndromes of neurodegeneration, such as ischemic and hemorrhagic stroke. 2,3)One cause for an elevation of intracellular ROS is thought to stem from an elevation of extracellular glutamate. 4) Excess extracellular glutamate can affect the influx of cystine into cells so reducing the rate of intracellular glutathione (GSH) formation 4) and in the process undermining a major cellular defense mechanism to maintain homeostatic levels of ROS. Mitochondria are a major target of ROS attack and at the same time is a source for ROS production such as the superoxide anion.5) Intracellular ROS levels in healthy cells therefore exist in a balanced redox state and over production as a consequence of an underlying pathogenic state leads to breakdown of homeostasis. Importantly, excess intracellular ROS can lead to a depletion of sulphur containing thiols. 4) In addition substances such as catalase, superoxid...

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Fenoldopam and N‐acetylcysteine for the Prevention of Radiographic Contrast Material—Induced Nephropathy: A Review

Cited by 17 publications

References 27 publications

Pathophysiology of contrast medium–induced nephropathy

Pathophysiology of contrast medium–induced nephropathy

N-Acetylcysteine Improves the Hemodynamics and Oxidative Stress in Hypoxic Newborn Pigs Reoxygenated With 100% Oxygen

Sulphur Antioxidants Inhibit Oxidative Stress Induced Retinal Ganglion Cell Death by Scavenging Reactive Oxygen Species but Influence Nuclear Factor (Erythroid-Derived 2)-Like 2 Signalling Pathway Differently

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