Role of intrinsic antioxidant enzymes in renal oxidant injury

Yoshioka, Toshimasa; Bills, Teresa; Moore-Jarrett, Tracy; Greene, Harry L.; Burr, Ian M.; Ichikawa, Iekuni

doi:10.1038/ki.1990.197

Cited by 118 publications

(56 citation statements)

References 24 publications

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“…Oxidant injury mediated by tert-butyl hydroperoxide is augmented by glutathione depletion and lessened when cellular levels of glutathione are increased (3 1-33). In vivo studies in rat kidneys suggest that antioxidant enzyme activity is an important determinant of oxidant-induced renal dysfunction (36). In this study, we confirm the role of the glutathione redox cycle in preventing lytic injury and we demonstrate a role for catalase as well as the glutathione redox cycle in protecting endothelial cells and epithelial cells from oxidant injury when a different indicator (ATP depletion) of oxidant injury is determined.…”

Section: Discussionsupporting

confidence: 71%

Antioxidant Defense Mechanisms of Endothelial Cells and Renal Tubular Epithelial Cells In Vitro: Role of the Glutathione Redox Cycle and Catalase

et al. 1992

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ABSTRACT. We recently demonstrated that endothelial cells are more susceptible than renal tubular epithelial cells to oxidant injury and that renal tubular epithelial cells with proximal tubular characteristics including porcine proximal tubular epithelial cells, opossum kidney proximal tubular epithelial cells, and normal human kidney cortical epithelial cells are more susceptible to oxidant injury than the distal nephron-derived Madin Darby canine kidney cell line. To determine the basis of this differential response, we evaluated several antioxidant defenses in the five cell lines. Glutathione levels were not significantly different among the five cell lines, but catalase and glutathione reductase levels were significantly (p < 0.01) lower in endothelial cells compared to all renal tubular epithelial cells. Among renal tubular epithelial cells, Madin Darby canine kidney cells had significantly (p < 0.05) higher glutathione peroxidase activity. To further evaluate the role of antioxidant defenses in limiting oxidant injury, we determined two responses to oxidant injury (ATP depletion and 51Cr release) when glutathione was depleted with buthionine sulfoxamine and when catalase was inhibited with aminotriazole. Oxidant-induced ATP depletion was accentuated when catalase was inhibited as well as when glutathione was depleted with buthionine sulfoxamine. In contrast, inhibition of catalase had little or no effect on 51Cr release, whereas glutathione depletion resulted in accentuated 5'Cr release. We conclude that the increased susceptibility of endothelial cells to oxidant injury as compared with epithelial cells is associated with lower antioxidant defenses. Disruption of the glutathione redox cycle results in accentuated ATP depletion and lytic injury, whereas inhibition of catalase results in accentuated ATP depletion with little effect on lytic injury. Augmented oxidant-induced ATP depletion without augmented cell lysis suggests that ATP depletion alone may not be a critical mediator of cell death in oxidant stress.

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Section: Discussionsupporting

confidence: 71%

Antioxidant Defense Mechanisms of Endothelial Cells and Renal Tubular Epithelial Cells In Vitro: Role of the Glutathione Redox Cycle and Catalase

et al. 1992

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“…• induction of antioxidant enzymes by ischemia-reperfusion injury protects against H 2 O 2 -induced proteinuria (126) • induction of antioxidant enzymes by glucocorticoids protects against PAN-induced proteinuria (127) Evidence for the role of oxidants in passive Heymann nephritis…”

Section: Animal Model Of Membranous Nephropathymentioning

confidence: 99%

Oxidants in Chronic Kidney Disease

Shah

Baliga

Rajapurkar

et al. 2007

Journal of the American Society of Nephrology

238

189

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Chronic kidney disease is a worldwide public health problem that affects approximately 10% of the US adult population and is associated with a high prevalence of cardiovascular disease and high economic cost. Chronic renal insufficiency, once established, tends to progress to end-stage kidney disease, suggesting some common mechanisms for ultimately causing scarring and further nephron loss. This review defines the term reactive oxygen metabolites (ROM), or oxidants, and presents the available experimental evidence in support of the role of oxidants in diabetic and nondiabetic glomerular disease and their role in tubulointerstitial damage that accompanies progression. It concludes by reviewing the limited human data that provide some proof of concept that the observations in experimental models may be relevant to human disease.

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“…Catalase activity, protein and/or mRNA levels have been found to be increased, [31][32][33] unchanged 34) or decreased [35][36][37][38][39][40][41][42] during oxidative stress. A ROS-mediated, biphasic model of catalase regulation has, however, been proposed in which catalase is stimulated by c-Abl/Arg-mediated phosphorylation at lower ROS levels, 43) while in the event of uncontrollable ROS levels, catalase is degraded by ubiquitinmediated proteasomal proteolysis, which thereby induces cell death.…”

Section: Discussionmentioning

confidence: 99%

Involvement of c-Met- and Phosphatidylinositol 3-Kinase Dependent Pathways in Arsenite-Induced Downregulation of Catalase in Hepatoma Cells

Kim

Lee

Kang

et al. 2011

Biological & Pharmaceutical Bulletin

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Cellular defense systems, including a variety of antioxidant molecules and enzymes such as superoxide dismutase, glutathione peroxidase and catalase, ensure that reactive oxygen species (ROS) are maintained at relatively low levels in normal conditions. 1) Arsenic and its compounds are welldocumented environmental toxicants 2) that induce oxidative damage by increasing the production of ROS. Oxidative damage has been suggested to play a key role in arsenicinduced toxicity. 3-7)Catalase protects cells from ROS-induced damage by catalyzing the breakdown of hydrogen peroxide (H 2 O 2 ) into oxygen and water. Arsenic has been demonstrated to decrease catalase expression both in animal tissues and cultured cells. Catalase activity is significantly decreased in the liver of rats treated with arsenite. [8][9][10] Arsenite treatment in vitro decreases catalase activity in human fibroblasts. 4) In a human keratinocyte cell line, it was also shown to decrease levels of catalase mRNA and protein. 11)Phosphatidylinositol 3-kinases (PI3Ks) are key components for the activation of Akt signaling. In the PI3K/Akt pathway, formation of 3-phosphoinositides by PI3K enables the activation of Akt by phosphoinositide-dependent protein kinases 1 and 2, which phosphorylate Akt at threonine residue 308 (Thr308) and serine residue 473 (Ser473), respectively. PI3K/Akt is thought to play a pivotal role in regulating cell proliferation, survival, metabolism and cancer progression. The PI3K/Akt pathway is downstream of c-Met receptor tyrosine kinase, a receptor for hepatocyte growth factor. [12][13][14] In c-Met-deficient mouse hepatocytes, the level of catalase protein is constitutively high, 15) suggesting that a cMet-dependent pathway is involved in catalase expression. Rat liver epithelial cells transformed by chronic exposure to arsenite show upregulated c-Met expression. Previous studies have demonstrated arsenite-induced activation of PI3K and c-Met-and PI3K-dependent inhibition of catalase expression. The aim of this study was to examine the involvement of c-Met-and PI3K-dependent pathways in arsenite-induced inhibition of catalase expression. Catalase mRNA and protein expression have been analyzed in human hepatoma cells treated with sodium arsenite and an inhibitor of either c-Met or PI3K. MATERIALS AND METHODS ChemicalsAll chemicals used were of reagent grade or higher and were obtained from Sigma-Aldrich (St. Louis, MO, U.S.A.), unless otherwise specified.Cell Treatment Human hepatoma cell line HepG2 was Seoul 156-756, Korea. Received July 13, 2011; accepted August 10, 2011; published

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Role of intrinsic antioxidant enzymes in renal oxidant injury

Cited by 118 publications

References 24 publications

Antioxidant Defense Mechanisms of Endothelial Cells and Renal Tubular Epithelial Cells In Vitro: Role of the Glutathione Redox Cycle and Catalase

Antioxidant Defense Mechanisms of Endothelial Cells and Renal Tubular Epithelial Cells In Vitro: Role of the Glutathione Redox Cycle and Catalase

Oxidants in Chronic Kidney Disease

Involvement of c-Met- and Phosphatidylinositol 3-Kinase Dependent Pathways in Arsenite-Induced Downregulation of Catalase in Hepatoma Cells

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