A role for oxygen free radicals in aminonucleoside nephrosis

Diamond, Jonathan R.; Bonventre, Joseph V.; Karnovsky, Morris J.

doi:10.1038/ki.1986.24

Cited by 232 publications

(128 citation statements)

References 20 publications

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“…Several facts may explain the alterations of MDA, vitamin C and E levels in INS. First, free radicals are possible mediators of injury in nephrosis by enhancing permeability of the glomerular capillary wall, 26 meanwhile, dyslipidemia of INS is known to be associated with oxidative stress. 12 Hence, MDA, by-product of lipid membranes peroxidation, would increase due to the above-mentioned mechanisms, similar results were observed in the active or remission stage of INS in our study.…”

Section: Discussionmentioning

confidence: 99%

Serum levels of malondialdehyde, vitamin C and E in idiopathic nephrotic syndrome: a meta-analysis

Mao¹,

Zhang²,

Huang³

2014

Renal Failure

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It is well documented that oxidative stress is involved in the pathogenesis of idiopathic nephrotic syndrome (INS). Malondialdehyde (MDA) is a measurement of lipid oxidation; vitamin C and E are important components of antioxidants. However, the association between MDA, vitamin C or E levels and INS remains elusive. A meta-analysis was performed to investigate the alteration of serum levels of MDA, vitamin C and E in INS compared with controls. Eight studies were included in our meta-analysis according to predefined criteria. Active INS patients demonstrated significantly higher level of serum MDA (SMD: 2.13, 95% CI: 1.511 to 2.749, p510 ) and similar level of serum vitamin E compared with those in controls. No significant publication bias was observed. In conclusion, the disorder of MDA and vitamin C persists in the remission stage of INS. It seems that the serum levels of vitamin C and E is associated with the responsiveness of INS to steroids. However, more studies should be performed in the future.

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Section: Discussionmentioning

confidence: 99%

Serum levels of malondialdehyde, vitamin C and E in idiopathic nephrotic syndrome: a meta-analysis

Mao¹,

Zhang²,

Huang³

2014

Renal Failure

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“…Importantly, a central role for XOR also has been demonstrated in a variety of clinical disorders and relevant animal models associated with oxidative stress or injury, including inflammation, infection, ischemic tissue injury, and various cancers (13)(14)(15)(16)(17)(18)(19)(20)(21)(22). In acute renal failure, endotoxin-induced mucosal injury, viral pneumonia, ischemia-reperfusion injury, and cutaneous photosensitivity to hematoporphyrins, excess XOR-derived ROS have been demonstrated to cause tissue injury (15)(16)(17)(18)(19)(20)(21)(22).…”

mentioning

confidence: 99%

Identification of Proteins Binding to E-Box/Ku86 Sites and Function of the Tumor Suppressor SAFB1 in Transcriptional Regulation of the Human Xanthine Oxidoreductase Gene

Lin

LaVallee

et al. 2008

Journal of Biological Chemistry

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The xanthine oxidoreductase gene (XOR) encodes an important source of reactive oxygen species and uric acid, and its expression is associated with various human diseases including several forms of cancer. We previously reported that basal human XOR (hXOR) expression is restricted or repressed by E-box and TATA-like elements and a cluster of transcriptional proteins, including AREB6-like proteins and DNA-dependent protein kinase (DNA-PK). We now demonstrate that the cluster contains the tumor suppressors SAFB1, BRG1, and SAF-A. We further demonstrate that SAFB1 silencing increases hXOR expression and that SAFB1 directly binds to the E-box. Multiple studies in vitro and in vivo including pulldown, immunoprecipitation and chromatin immunoprecipitation analyses indicate that SAFB1, Ku86, and BRG1 associate with each other. The results suggest that the SAFB1 complex binds to the hXOR promoter in a chromatin environment and plays a critical role in restricting hXOR expression via its direct interaction with the E-box, DNA-PK, and tumor suppressors. Moreover, we demonstrate that the cytokine, oncostatin M (OSM), induces the phosphorylation of SAFB1 and that the OSM-induced hXOR mRNA expression is significantly inhibited by silencing the DNA-PK catalytic subunit or SAFB1 expression. The present studies for the first time demonstrate that hXOR is a tumor suppressor-targeted gene and that the phosphorylation of SAFB1 is regulated by OSM, providing a molecular basis for understanding the role of SAFB1-regulated hXOR transcription in cytokine stimulation and tumorigenesis.

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“…Oxidants have been implicated in the pathogenesis of a number of renal diseases including ischaemia/reperfusion injury, aminonucleoside nephrosis, gentamicin nephrotoxicity, and acute nephrotoxic nephritis (Paller et al 1984;Rehan et al 1984;Baud & Ardaillou 1986;Diamond et al 1986;Walker & Shah 1988). While the importance of oxidants in the pathogenesis of experimental renal injury has been established, the cellular mechanisms that result in the cell death remain uncertain (Baliga et al 1999).…”

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confidence: 99%

Oxidant‐Induced Cell Death in Renal Epithelial Cells: Differential Effects of Inorganic and Organic Hydroperoxides

Park

Jung

Koak

et al. 2003

Pharmacology & Toxicology

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This study was undertaken in order to examine the roles of lipid peroxidation and poly (ADP-ribose) polymerase (PARP) activation in oxidant-induced renal cell death. Opossum kidney cell cultures were used as the renal epithelial cell model, and an inorganic hydroperoxide H 2 O 2 and an organic hydroperoxide t-butylhydroperoxide were employed as model oxidants. Cell death by both oxidants could be prevented by thiols (dithiothreitol and glutathione), iron chelators (deferoxamine and phenanthroline), and hydroxyl radical scavengers (dimethylthiourea and pyruvate). Phenolic antioxidants N,Nø-diphenyl-p-phenylenediamine (DPPD) and butylated hydroxyanisole had no effect on the H 2 O 2 -induced cell death . However, the t-butylhydroperoxide-induced cell death was effectively prevented by these antioxidants. The PARP inhibitor 3-aminobenzamide prevented the cell death induced by H 2 O 2 , but not cell death by t-butylhydroperoxide. The PARP activity was increased in cells exposed to H 2 O 2 but not t-butylhydroperoxide. Unlike in opossum kidney cells, in rabbit renal cortical slices both oxidants H 2 O 2 and t-butylhydroperoxide induced cell death through a lipid peroxidation-dependent and PARP-independent mechanism. Effects of DPPD and 3-aminobenzamide on H 2 O 2 -induced cell death in primary cultured rabbit proximal tubular cells were similar to those in opossum kidney cells. These results indicate that 1) the H 2 O 2 -induced cell death in cultured renal epithelial cells is associated with PARP activation but not lipid peroxidation, whereas the t-butylhydroperoxide-induced cell death is mediated by lipid peroxidation, and 2) the role of lipid peroxidation in H 2 O 2 cytotoxicity may be different between freshly isolated renal tubular cells and cultured renal epithelial cells.

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A role for oxygen free radicals in aminonucleoside nephrosis

Cited by 232 publications

References 20 publications

Serum levels of malondialdehyde, vitamin C and E in idiopathic nephrotic syndrome: a meta-analysis

Serum levels of malondialdehyde, vitamin C and E in idiopathic nephrotic syndrome: a meta-analysis

Identification of Proteins Binding to E-Box/Ku86 Sites and Function of the Tumor Suppressor SAFB1 in Transcriptional Regulation of the Human Xanthine Oxidoreductase Gene

Oxidant‐Induced Cell Death in Renal Epithelial Cells: Differential Effects of Inorganic and Organic Hydroperoxides

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