Reactive oxygen species and acute renal failure

Nath, Karl A.; Norby, Suzanne M.

doi:10.1016/s0002-9343(00)00612-4

Cited by 380 publications

(333 citation statements)

References 94 publications

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“…8I) would corroborate the data of D-glucoseinduced up-regulation of RSOR͞MIOX. Here, it is worth pointing out a potential paradox that a decreased RSOR͞MIOX expression has been reported in acute renal failure (39), where tubular cells are under extreme oxidant stress (40). It may be that expression of the enzyme depends on the degree or type of oxidant stress (cytosolic vs. membrane vs. mitochondrial); nevertheless, it seems that OxREs are functionally active in RSOR͞MIOX promoter.…”

Section: Discussionmentioning

confidence: 95%

Modulation of renal-specific oxidoreductase/ myo -inositol oxygenase by high-glucose ambience

Nayak¹,

Xie²,

Akagi³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Biological properties of renal-specific oxidoreductase (RSOR), characteristics of its promoter, and underlying mechanisms regulating its expression in diabetes were analyzed. RSOR expression, normally confined to the renal cortex, was markedly increased and extended into the outer medullary tubules in db͞db mice, a model of type 2 diabetes. Exposure of LLCPK cells to D-glucose resulted in a dose-dependent increase in RSOR expression and its enzymatic activity. The latter was related to one of the glycolytic enzymes, myo-inositol oxygenase. The increase in activity was in proportion to serum glucose concentration. The RSOR expression also increased in cells treated with various organic osmolytes, e.g., sorbitol, myoinositol, and glycerolphosphoryl-choline and H 2O2. Basal promoter activity was confined to ؊1,252 bp upstream of ATG, and it increased with the treatment of high glucose and osmolytes. EMSAs indicated an increased binding activity with osmotic-, carbohydrate-, and oxidant-response elements in cells treated with high glucose and was abolished by competitors. Supershifts, detected by anti-nuclear factor of activated T cells, and carbohydrate-response-element-binding protein established the binding specificity. Nuclear factor of activated T cells tonicityenhancer-binding protein and carbohydrate-response-elementbinding protein had increased nuclear expression in cells treated with high glucose. The activity of osmotic-response element exhibited a unique alternate binding pattern, as yet unreported in osmoregulatory genes. Data indicate that RSOR activity is modulated by diverse mechanisms, and it is endowed with dual properties to channel glucose intermediaries, characteristic of hepatic aldehyde reductases, and to maintain osmoregulation, a function of renal medullary genes, e.g., aldose reductase, in diabetes. diabetic nephropathy ͉ hyperglycemia ͉ osmoregulation D iabetic nephropathy is characterized by hyperplasia͞ hypertrophy of intrinsic renal cells and increased extracellular matrices (1). These changes are related to the increased cellular flux of glucose intermediaries (2), de novo synthesis of intra-and extracellular advanced glycation end products (3, 4), activation of protein kinase C (5, 6), increased expression of transforming growth factor-␤ (7), increased activity of GTP-binding and cell-cycle proteins (6,8), and generation of reactive oxygen species (9, 10), with consequential compromise in renal functions (11,12). Such complex interrelated cellular signaling events, also involving various forms of MAP͞ERK kinases and Smad proteins, have been defined mainly in glomerular cells (13,14); information relevant to the tubulointerstitial cells, although notably affected, is limited (15, 16). Conceivably, cellular changes in the tubulointerstitium parallel those in the glomerulus, with scarring and thickening of the basement membranes, and they correlate relatively better with the derangements in renal functional parameters (17, 18). Thus, much attention is warranted to the understanding of the...

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Section: Discussionmentioning

confidence: 95%

Modulation of renal-specific oxidoreductase/ myo -inositol oxygenase by high-glucose ambience

Nayak¹,

Xie²,

Akagi³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…Both NDK B and NDK A are modified after H 2 O 2 treatment [26] , and Cys 109 of NDK A was identified as the site of oxidative modification by ROS [27] . Because Cys 109 is also present in NDK B and no other PTM of NDK B has been reported, the basic isoform of NDK B also seems to be subject to oxidative modification under physiological conditions, which would support the existence of a higher ROS level in the kidney than in other tissues [13] . Altered NDK expression is associated with the inhibition of cellular proliferation and apoptosis [28] , and NDK B overexpression reduces H 2 O 2 -induced cell death in BAF3 cells [29] .…”

Section: Protein Involved In Cellular Energeticsmentioning

confidence: 97%

“…Oxidative stress is a pathway for renal injury [13] . To investigate whether the renal damage induced by ASB is caused by ROS, the levels of SOD and MDA in the renal tissue were analyzed (Figure 1, 2).…”

Section: Index Of Renal Oxidationmentioning

confidence: 99%

“…Although further study is needed to identify the PTM of NDUFA10 in the mouse kidney, the partial inhibition of the PTM of NDUFA10 upon treatment with ASB suggests aberrant superoxide generation by complex I. Excessive endogenous ROS can contribute to acute renal injury [13] . Hence, the ASB-induced changes in the PTM of NDUFA10 might contribute to ASB nephrotoxicity.…”

Section: Protein Involved In Cellular Energeticsmentioning

confidence: 99%

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Proteomic alterations in mouse kidney induced by andrographolide sodium bisulfite

et al. 2011

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Aim: To identify the key proteins involved in the nephrotoxicity induced by andrographolide sodium bisulfite (ASB). Methods: Male ICR mice were intravenously administrated with ASB (1000 or 150 mg·kg -1 ·d -1 ) for 7 d. The level of malondialdehyde (MDA) and the specific activity of superoxide dismutase (SOD) in kidneys were measured. The renal homogenates were separated by two-dimensional electrophoresis, and the differential protein spots were identified using a matrix-assisted laser desorption/ionization (MALDI) time-of-flight (TOF)/TOF mass spectrometry. Results: The high dose (1000 mg/kg) of ASB significantly increased the MDA content, but decreased the SOD activity as compared to the control mice. The proteomic analysis revealed that 6 proteins were differentially expressed in the high-dose group. Two stressresponsive proteins, ie heat shock cognate 71 kDa protein (HSC70) and peroxiredoxin-6 (PRDX6), were regulated at the expression level. The remaining 4 proteins involving in cellular energy metabolism, including isoforms of methylmalonyl-coenzyme A mutase (MUT), nucleoside diphosphate-linked moiety X motif 19 (Nudix motif19), mitochondrial NADH dehydrogenase 1 alpha subcomplex subunit 10 (NDUFA10) and nucleoside diphosphate kinase B (NDK B), were modified at the post-translational levels. Conclusion: Our findings suggest that the mitochondrion is the primary target of ASB and that ASB-induced nephrotoxicity results from oxidative stress mediated by superoxide produced by complex I.

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“…The main compounds are the superoxide anion, hydrogen peroxide and the hydroxyl radical. Nitric oxide and the peroxynitrite radical also present the capacity to induce oxidation damage 2 . Kidneys are responsible for 10% of the body oxygen consumption.…”

Section: Introductionmentioning

confidence: 99%

Prevention of renal ischemia/reperfusion injury in rats using acetylcysteine after anesthesia with isoflurane

et al. 2012

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PURPOSE: To evaluate the effect of N-acetylcysteine, as a renoprotective agent, when administered early after anesthesia induction, against ischemia/reperfusion injury in rats anesthetized with isoflurane. METHODS: Eighteen male Wistar rats weighing > 300g were anesthetized with isoflurane. The internal jugular vein and the left carotid artery were dissected and cannulated. The animals were randomly divided into GAcetyl, receiving intravenous N-acetylcysteine, 300mg/kg, and GIsot, isotonic saline. After 30 minutes, right nephrectomy was performed and the left renal artery was clamped during 45 minutes. The animals were sacrificed after 48 hours and blood samples were taken after anesthetic induction and upon sacrificing of the animals to evaluate blood creatinine. The kidneys were sent for histological analysis. RESULTS: The variation in serum creatinine was 2.33mg/dL ± 2.21 in GAcetyl and 4.38mg/dL ± 2.13 in GIsot (p=0.074). Two animals presented intense tubular necrosis in GAcetyl, compared to 5 in GIsot. Only GAcetyl presented animals free of tubular necrosis (two) and tubular degeneration (one). CONCLUSION: After renal ischemia/reperfusion, the rats which were given N-acetylcysteine presented less variation in serum creatinine and milder kidney injuries than the control group.

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Reactive oxygen species and acute renal failure

Cited by 380 publications

References 94 publications

Modulation of renal-specific oxidoreductase/ myo -inositol oxygenase by high-glucose ambience

Modulation of renal-specific oxidoreductase/ myo -inositol oxygenase by high-glucose ambience

Proteomic alterations in mouse kidney induced by andrographolide sodium bisulfite

Prevention of renal ischemia/reperfusion injury in rats using acetylcysteine after anesthesia with isoflurane

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