Cellular Oxidative Processes in Relation to Renal Disease

Wardle, E. N.

doi:10.1159/000083477

Cited by 44 publications

(42 citation statements)

References 198 publications

(118 reference statements)

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“…The major sources of intracellular ROS are the mitochondria, the NADPH-and xanthine-oxidase systems [17]. Our previous study suggests that a major part of Ch-NIC-and oxidant injury-induced intracellular ROS originates in the mitochondria [6].…”

Section: Discussionmentioning

confidence: 98%

“…Our recent data showed that Ch-NIC may exacerbate IR-AKI-induced oxidative stress by increasing the production of reactive oxygen species (ROS) in proximal tubule cells [6]. While the major sources of intracellular ROS are the mitochondria, the nicotinamide adenine dinucleotide phosphate (NADPH)-and xanthine-oxidase systems [17], our previous study suggests that a major part of Ch-NIC and oxidant injury-induced intracellular ROS originates in the mitochondria [6]. Indeed, Ch-NIC adversely affects mitochondrial function and mitochondrial ROS production [18,19]; however, the mechanism by which it does so is unknown.…”

Section: Introductionmentioning

confidence: 99%

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Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc

Arany

Clark

Reed

et al. 2013

Nephrology Dialysis Transplantation

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc

Arany

Clark

Reed

et al. 2013

Nephrology Dialysis Transplantation

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“…When redox homeostasis transitions to redox stress, redox signaling ensues in all tissues and organs regardless of the multiple similar or dissimilar etiologies due to redox stress being a redox signaling system [17, 18]. An elegant discussion of the cellular oxidative processes in renal disease has recently been published for a more in-depth view of these complex mechanisms [19]. …”

Section: Redox Stressmentioning

confidence: 99%

Renal Redox Stress and Remodeling in Metabolic Syndrome, Type 2 Diabetes mellitus, and Diabetic Nephropathy: Paying Homage to the Podocyte

Hayden¹,

Whaley‐Connell²,

Sowers³

2005

Am J Nephrol

109

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Type 2 diabetes mellitus has reached epidemic proportions and diabetic nephropathy is the leading cause of end-stage renal disease. The metabolic syndrome constitutes a milieu conducive to tissue redox stress. This loss of redox homeostasis contributes to renal remodeling and parallels the concurrent increased vascular redox stress associated with the cardiometabolic syndrome. The multiple metabolic toxicities, redox stress and endothelial dysfunction combine to weave the complicated mosaic fabric of diabetic glomerulosclerosis and diabetic nephropathy. A better understanding may provide both the clinician and researcher tools to unravel this complicated disease process. Cellular remodeling of podocyte foot processes in the Ren-2 transgenic rat model of tissue angiotensin II overexpression (TG(mREN-2)27) and the Zucker diabetic fatty model of type 2 diabetes mellitus have been observed in preliminary studies. Importantly, angiotensin II receptor blockers have been shown to abrogate these ultrastructural changes in the foot processes of the podocyte in preliminary studies. An integrated, global risk reduction, approach in therapy addressing the multiple metabolic abnormalities combined with attempts to reach therapeutic goals at an earlier stage could have a profound effect on the development and progressive nature to end-stage renal disease and ultimately renal replacement therapy.

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“…In human uremic patients, a state of imbalance between pro‐oxidative and antioxidative processes has been established, and defined as oxidative stress with increased amounts of reactive oxygen species (ROS) present 3, 4, 5. ROS are involved in cell signaling and cause activation of proinflammatory and mitogenic cellular pathways, which enhance the progression of renal fibrosis and cause a progressive decline in renal function 5, 6, 7. Glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and nitric oxide synthase are the most important antioxidant enzymes that detoxify ROS molecules in the kidneys 4…”

mentioning

confidence: 99%

Plasma and Erythrocyte Glutathione Peroxidase Activity, Serum Selenium Concentration, and Plasma Total Antioxidant Capacity in Cats with IRIS Stages I–IV Chronic Kidney Disease

Žel

Tozon

Svete

2013

Veterinary Internal Medicne

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BackgroundSerum selenium concentrations and the activity of plasma glutathione peroxidase (GPx) decrease with the progression of chronic kidney disease (CKD) in human patients. Selenium is considered a limiting factor for plasma GPx synthesis. Plasma total antioxidant capacity (TAC) is decreased in CKD cats in comparison to healthy cats.HypothesisSerum selenium concentrations and plasma and erythrocyte GPx activity in cats with CKD are lower than in healthy cats. Serum selenium concentrations, the activity of enzymes, and plasma TAC progressively decrease with the progression of kidney disease according to IRIS (International Renal Interest Society) classification.AnimalsTwenty‐six client‐owned cats in IRIS stages I–IV of CKD were compared with 19 client‐owned healthy cats.MethodsA CBC, serum biochemical profile, urinalysis, plasma and erythrocyte GPx activity, serum selenium concentration, and plasma TAC were measured in each cat.ResultsCats in IRIS stage IV CKD had a significantly higher (P = .025) activity of plasma GPx (23.44 ± 6.28 U/mL) than cats in the control group (17.51 ± 3.75 U/mL). There were no significant differences in erythrocyte GPx, serum selenium concentration, and plasma TAC, either among IRIS stages I–IV CKD cats or between CKD cats and healthy cats.Conclusions and Clinical ImportanceErythrocyte GPx activity, serum selenium concentration, and plasma TAC do not change in CKD cats compared with healthy cats. Selenium is not a limiting factor in feline CKD. Increased plasma GPx activity in cats with stage IV CKD suggests induction of antioxidant defense mechanisms. Antioxidant defense systems might not be exhausted in CKD in cats.

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Cellular Oxidative Processes in Relation to Renal Disease

Cited by 44 publications

References 198 publications

Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc

Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc

Renal Redox Stress and Remodeling in Metabolic Syndrome, Type 2 Diabetes mellitus, and Diabetic Nephropathy: Paying Homage to the Podocyte

Plasma and Erythrocyte Glutathione Peroxidase Activity, Serum Selenium Concentration, and Plasma Total Antioxidant Capacity in Cats with IRIS Stages I–IV Chronic Kidney Disease

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