Oxidative stress and dysregulation of NAD(P)H oxidase and antioxidant enzymes in diet-induced metabolic syndrome

Roberts, Christian K.; Barnard, R. James; Sindhu, Ram K.; Jurczak, Michael J.; Ehdaie, Ashkan; Vaziri, Nosratola D.

doi:10.1016/j.metabol.2006.02.022

Cited by 281 publications

(223 citation statements)

References 41 publications

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“…Overexpression or exogenous administration of Cu/Zn-SOD ameliorated ischemia-reperfusion injury of the kidneys, heart, and brain, suggesting a pathogenic role for the suppression of Cu/Zn-SOD (7,8,38,48,53). Downregulation of Cu/Zn-SOD in association with increased oxidative stress in the kidney was seen in several other experimental diseases models, including a chronic kidney failure model of the remnant kidney (45), carboplatin nephrotoxicity (18), and the metabolic syndrome (34). Furthermore, recent proteomic , and infliximab-treated RAS kidney (C).…”

Section: Discussionmentioning

confidence: 99%

Chronic hypoxia aggravates renal injury via suppression of Cu/Zn-SOD: a proteomic analysis

Son¹,

Kojima²,

Inagi³

et al. 2008

American Journal of Physiology-Renal Physiology

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Son D, Kojima I, Inagi R, Matsumoto M, Fujita T, Nangaku M. Chronic hypoxia aggravates renal injury via suppression of Cu/Zn-SOD: a proteomic analysis. Am J Physiol Renal Physiol 294: F62-F72, 2008. First published October 24, 2007 doi:10.1152/ajprenal.00113.2007.-Accumulating evidence suggests a pathogenic role of chronic hypoxia in various kidney diseases. Chronic hypoxia in the kidney was induced by unilateral renal artery stenosis, followed 7 days later by observation of tubulointerstitial injury. Proteomic analysis of the hypoxic kidney found various altered proteins. Increased proteins included lipocortin-5, calgizzarin, ezrin, and transferrin, whereas the decreased proteins were ␣ 2u-globulin PGCL1, eukaryotic translation elongation factor 1␣ 2, and Cu/Zn superoxide dismutase (SOD1). Among these proteins, we focused on Cu/Zn-SOD, a crucial antioxidant. Western blot analysis and real-time quantitative PCR analysis confirmed the downregulation of Cu/Zn-SOD in the chronic hypoxic kidney. Furthermore, our laser capture microdissection system showed that the expression of Cu/Zn-SOD was predominant in the tubulointerstitium and was decreased by chronic hypoxia. The tubulointerstitial injury estimated by histology and immunohistochemical markers was ameliorated by tempol, a SOD mimetic. This amelioration was associated with a decrease in levels of the oxidative stress markers 4-hydroxyl-2-nonenal and nitrotyrosine. Our in vitro studies utilizing cultured tubular cells revealed a role of TNF-␣ in downregulation of Cu/Zn-SOD. Since the administration of anti-TNF-␣ antibody ameliorated Cu/Zn-SOD suppression, TNF-␣ seems to be one of the suppressants of Cu/Zn-SOD. In conclusion, our proteomic analysis revealed a decrease in Cu/Zn-SOD, at least partly by TNF-␣, in the chronic hypoxic kidney. This study, for the first time, uncovered maladaptive suppression of Cu/Zn-SOD as a mediator of a vicious cycle of oxidative stress and subsequent renal injury induced by chronic hypoxia. chronic kidney failure; oxidative stress ONCE RENAL DAMAGE REACHES a certain threshold, the progression of renal disease is consistent, irreversible and largely independent of the initial insult. The final common pathway in this process has been closely studied. The chronic hypoxia hypothesis, proposed by Fine et al. (11), emphasizes chronic ischemic damage in the tubulointerstitium as a final common pathway in end-stage kidney injury. Since its introduction, this fascinating hypothesis has been intensively investigated by many investigators (9,20,24). Despite intensive efforts to elucidate the pathomechanisms of chronic hypoxia on kidney damage, however, their complexity has hampered investigations and details remain scarce. Among others, mechanisms proposed to date include transdifferentiation (22), cell death (40 -42), production of extracellular matrix (26,27), and so on.Advances in proteomics technology offer promise to substantially improve our understanding and treatment of the molecular basis of disease. In particular, deciphering the a...

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Section: Discussionmentioning

confidence: 99%

Chronic hypoxia aggravates renal injury via suppression of Cu/Zn-SOD: a proteomic analysis

Son¹,

Kojima²,

Inagi³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…Rats fed a high-fat diet develop obesity, insulin resistance, and hypertension via an increase in NAD(P)H oxidase activity in the kidney, as seen in other animal models (273), and this contributes to endothelial dysfunction via oxidant degradation of NO (112).…”

Section: Fig 5 Schematic Showing the Link Between Cardiometabolic Smentioning

confidence: 94%

Redox Control of Renal Function and Hypertension

Nistala

Whaley‐Connell

Sowers

2008

Antioxidants & Redox Signaling

139

123

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“…This leads to excessive production of ROS in hyperglycemia, insulin resistance (due to cell respiration disorders) and obesity (a positive correlation was demonstrated between the volume of adipose tissue and the rate of ROS production), which are elements of MS. Thus, subjects with MS are particularly exposed to excessive ROS and they require special care in the range of efficient functioning of the antioxidant barrier [5,6].…”

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confidence: 99%

Lower Plasma Levels of Antioxidant Vitamins in Patients with Metabolic Syndrome: A Case Control Study

Godala¹,

Materek-Kuśmierkiewicz²,

Moczulski³

et al. 2016

Adv Clin Exp Med

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blood pressure or hypertension treatment, fasting hyperglycemia or diagnosed type 2 diabetes, abnormal lipid profile (hypertriglyceridemia and/or low HDL-cholesterol) A -research concept and design; B -collection and/or assembly of data; C -data analysis and interpretation; D -writing the article; E -critical revision of the article; F -final approval of article AbstractBackground. Metabolic syndrome (MS) is a coexistence of metabolic risk factors affecting the development of cardiovascular diseases. Reactive oxygen species, which are excessively produced in MS, participate in its pathogenesis. Vitamins A, C and E are an important part of the non-enzymatic antioxidative barrier in humans. Objectives. The aim of the study was to estimate plasma vitamin A, C and E levels and the intake of these vitamins from the diet in patients with MS. Material and Methods. The study included 182 patients with MS, 94 men and 88 women, aged 30-65 years (mean 57.31 ± 8.28 years). The control group was comprised of 91 subjects, 56 men and 35 women, aged 41-65 years (mean 57.75 ± 5.84 years). The MS diagnosis was based on IDF criteria. The determination of the serum level of vitamin A, C and E was performed using the spectrophotometric method. The food intake was assessed by 24-h dietary recall. Results. The mean plasma vitamin A, C and E levels were significantly lower in MS patients than in the controls (p = 0.05). No correlation was found between vitamin A, C and E intake from the diet and their plasma concentrations in MS patients. Plasma vitamin A, C and E deficiency was observed significantly more often in MS patients than in the control group (15.38% vs. 2.19%, 79.12% vs. 8.79% and 60.45% vs. 5.49%, p < 0.0001, respectively). BMI was the one factor significantly affecting the mean value of vitamin A, C and E levels in MS patients. Conclusions. MS patients demonstrated significantly lower plasma levels of vitamin A, C and E compared to the healthy subjects. Lower plasma levels of antioxidant vitamins with their high intake from the diet indicate antioxidant barrier impairment in MS patients (Adv Clin Exp Med 2016, 25, 4, 689-700).

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Oxidative stress and dysregulation of NAD(P)H oxidase and antioxidant enzymes in diet-induced metabolic syndrome

Cited by 281 publications

References 41 publications

Chronic hypoxia aggravates renal injury via suppression of Cu/Zn-SOD: a proteomic analysis

Chronic hypoxia aggravates renal injury via suppression of Cu/Zn-SOD: a proteomic analysis

Redox Control of Renal Function and Hypertension

Lower Plasma Levels of Antioxidant Vitamins in Patients with Metabolic Syndrome: A Case Control Study

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