Oxidant mechanisms in toxic acute renal failure

Baliga, Radhakrishna; Ueda, Norishi; Walker, Patrick D.; Shah, Sudhir V.

doi:10.1016/s0272-6386(97)90212-2

Cited by 310 publications

(201 citation statements)

References 49 publications

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“…This drug is widely used to treat autoimmune diseases, being associated with reduction in the number of hospitalization days for transplanted patients and for rejection episodes (Rezzani 2004). However, several side effects are associated with CsA treatment such as: nephrotoxicity (Bertani et al 1987, Baliga et al 1997, Fellstrom 2004, Rezzani 2004, Hagar et al 2006, Josephine et al 2006, Rezzani et al 2006b), hepatotoxicity (Durak 370 KARINE M. DE FREITAS et al et al 2004, Hagar 2004, Rezzani 2004, 2006, Kurus et al 2008, Bohmer et al 2011, testicular dysfunction (Monteiro et al 2008) and damages to the ventral prostate (Freitas et al 2012a). Most of these are related to the increase of reactive oxygen species (Wolf et al 1997, Buffoli et al 2005, Rezzani 2006, causing damage to tissue structure and functional disorders (Whiting et al 1983).…”

Section: Introductionmentioning

confidence: 99%

The effects of Cyclosporin A and Heteropterys tomentosaon the rat liver

Freitas

Almeida

Monteiro

et al. 2015

An. Acad. Bras. Ciênc.

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Cyclosporin A (CsA) is a widely employed immunosuppressive drug that is associated with several side effects, among then hepatotoxicity. Heteropterys tomentosa is a Brazilian plant efficient in reducing damage caused by CsA on the rat testis and prostate. The aim of this study was to evaluate the effect of CsA and H. tomentosa (administered isolated or simultaneously) on the liver of Wistar rats. The animals were treated daily with water (control), CsA (15mg/kg/day), H. tomentosa infusion or CsA+H. tomentosa, for 21 or 56 days. The treatments did not alter liver morphology or cause fibrosis. H. tomentosa administered for 21 days increased the number of hepatocyte nuclei and Kupffer cell volumetric proportion. After 56 days of treatment, H. tomentosa administration did not alter the parameters analyzed. Biochemical plasma dosages and liver stereology showed impairment caused by CsA-treatment after 21 days; these results were not observed after 56 days of treatment. The simultaneous treatment with CsA and H. tomentosa for 21 or 56 days did not alleviate nor accentuate CsA hepatic effects. The present study showed that the 21 days treatment with CsA caused more alteration to the liver than the 56 days treatment; this could be related to hepatic recovery after the long term treatment.

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Section: Introductionmentioning

confidence: 99%

The effects of Cyclosporin A and Heteropterys tomentosaon the rat liver

Freitas

Almeida

Monteiro

et al. 2015

An. Acad. Bras. Ciênc.

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“…The hallmark of cisplatin nephrotoxicity is damage to the S3 segment of the proximal tubules. A number of pathways critical to nephrotoxicity have been identified, including endoplasmic reticulum stress ), metabolism via cysteine-S-conjugate β-lyase (Townsend et al 2003), oxidative damage (Baliga et al 1999), and renal inflammation, most notably mediated by tumor necrosis factor alpha (TNF-α Ramesh and Reeves 2002). Amifostine may attenuate cisplatin/ifosfamide nephrotoxicity in patients with solid tumors (Hartmann et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of cisplatin nephrotoxicity by inhibition of soluble epoxide hydrolase

et al. 2008

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Cisplatin is a highly effective chemotherapeutic agent against many tumors; however, it is also a potent nephrotoxicant. Given that there have been no significant advances in our ability to clinically manage acute renal failure since the advent of dialysis, the development of novel strategies to ablate nephrotoxicity would represent a significant development. In this study, we investigated the ability of an inhibitor of soluble epoxide hydrolase (sEH), n-butyl ester of 12-(3-adamantan-1-yl-ureiido)-dodecanoic acid (nbAUDA), to attenuate cisplatin-induced nephrotoxicity. nbAUDA is quickly converted to AUDA and results in maintenance of high AUDA levels in vivo. Subcutaneous administration of 40 mg/kg of nbAUDA to C3H mice every 24 h resulted in elevated blood levels of AUDA; this protocol was also associated with attenuation of nephrotoxicity induced by cisplatin (intraperitoneal injection) as assessed by BUN levels and histological evaluation of kidneys. This is the first report of the use of sEH inhibitors to protect against acute nephrotoxicity and suggests a therapeutic potential of these compounds.

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“…1,2 In response to injury, the kidney is able to elicit adaptive and protective mechanisms to limit further damage. One such mechanism is the rapid and robust induction of heme oxygenase-1 (HO-1).…”

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confidence: 99%

Heme Oxygenase-1 Inhibits Renal Tubular Macroautophagy in Acute Kidney Injury

Bolisetty

Traylor²,

Kim³

et al. 2010

Journal of the American Society of Nephrology

143

125

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Autophagy is a tightly regulated, programmed mechanism to eliminate damaged organelles and proteins from a cell to maintain homeostasis. Cisplatin, a chemotherapeutic agent, accumulates in the proximal tubules of the kidney and causes dose-dependent nephrotoxicity, which may involve autophagy. In the kidney, cisplatin induces the protective antioxidant heme oxygenase-1 (HO-1). In this study, we examined the relationship between autophagy and HO-1 during cisplatin-mediated acute kidney injury (AKI). In wild-type primary proximal tubule cells (PTC), we observed a time-dependent increase in autophagy after cisplatin. In HO-1 Ϫ/Ϫ PTC, however, we observed significantly higher levels of basal autophagy, impaired progression of autophagy, and increased apoptosis after cisplatin. Restoring HO-1 expression in these cells reversed the autophagic response and inhibited apoptosis after treatment with cisplatin. In vivo, although both wild-type and HO-1-deficient mice exhibited autophagosomes in the proximal tubules of the kidney in response to cisplatin, HO-1-deficient mice had significantly more autophagosomes, even in saline-treated animals. In addition, ecdysone-induced overexpression of HO-1 in cells led to a delay in autophagy progression, generated significantly lower levels of reactive oxygen species, and protected against cisplatin cytotoxicity. These findings demonstrsate that HO-1 inhibits autophagy, suggesting that the heme oxygenase system may contain therapeutic targets for AKI.

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Oxidant mechanisms in toxic acute renal failure

Cited by 310 publications

References 49 publications

The effects of Cyclosporin A and Heteropterys tomentosaon the rat liver

The effects of Cyclosporin A and Heteropterys tomentosaon the rat liver

Attenuation of cisplatin nephrotoxicity by inhibition of soluble epoxide hydrolase

Heme Oxygenase-1 Inhibits Renal Tubular Macroautophagy in Acute Kidney Injury

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