Sulforaphane protects against cisplatin-induced nephrotoxicity

Guerrero-Beltrán, Carlos Enrique; Calderón‐Oliver, Mariel; Tapia, Edilia; Medina-Campos, Omar Noel; Sánchez-González, Dolores Javier; Martínez-Martínez, Claudia María; Ortiz-Vega, Karla Mariana; Franco, Martha; Pedraza‐Chaverrí, José

doi:10.1016/j.toxlet.2009.11.007

Cited by 90 publications

(44 citation statements)

References 24 publications

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“…Catalase (CAT) activity was assayed in renal cortex by a method based on the disappearance of H 2 O 2 at 240 nm and glutathione peroxidase (GPx) activity was measured, in blood plasma and renal cortex, by the disappearance of NADPH at 340 nm in a reaction coupled with the enzyme GR [33]. …”

Section: Methodsmentioning

confidence: 99%

Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection

Negrette-Guzmán

Huerta-Yépez²,

Medina-Campos³

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Sulforaphane (SFN), an isothiocyanate naturally occurring in Cruciferae, induces cytoprotection in several tissues. Its protective effect has been associated with its ability to induce cytoprotective enzymes through an Nrf2-dependent pathway. Gentamicin (GM) is a widely used antibiotic; nephrotoxicity is the main side effect of this compound. In this study, it was investigated if SFN is able to induce protection against GM-induced nephropathy both in renal epithelial LLC-PK1 cells in culture and in rats. SFN prevented GM-induced death and loss of mitochondrial membrane potential in LLC-PK1 cells. In addition, it attenuated GM-induced renal injury (proteinuria, increases in serum creatinine, in blood urea nitrogen, and in urinary excretion on N-acetyl-β-D-glucosaminidase, and decrease in creatinine clearance and in plasma glutathione peroxidase activity) and necrosis and apoptosis in rats. The apoptotic death was associated with enhanced active caspase-9. Caspase-8 was unchanged in all the studied groups. In addition, SFN was able to prevent GM-induced protein nitration and decrease in the activity of antioxidant enzymes catalase and glutathione peroxidase in renal cortex. In conclusion, the protective effect of SFN against GM-induced acute kidney injury could be associated with the preservation in mitochondrial function that would prevent the intrinsic apoptosis and nitrosative stress.

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Section: Methodsmentioning

confidence: 99%

Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection

Negrette-Guzmán

Huerta-Yépez²,

Medina-Campos³

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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“…The method is based on the formation of a colored complex between MDA and 4-HNE with 1-methyl-2-phenylindole. Optical density was measured at 586 nm after 1 h of incubation at 45°C [30]. Data were expressed as nmol MDA and 4-HNE/mg protein.…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Curcumin Protects from Cardiac Reperfusion Damage by Attenuation of Oxidant Stress and Mitochondrial Dysfunction

et al. 2011

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This study was designed to investigate whether the pretreatment with curcumin, a yellow pigment from turmeric (Curcuma longa) known for its potent antioxidant capacity, was able to protect against the oxidant damage and mitochondrial dysfunction induced by reperfusion injury in isolated hearts. Rats were treated with a daily intragastric dose of curcumin (200 mg/kg) for 7 days prior to experimental ischemia (30 min) and reperfusion (60 min) (I/R). Cardiac mechanical work was measured during periods of stabilization, ischemia, and reperfusion. Oxidant stress and activity of antioxidant enzymes were measured in both homogenates of cardiac tissue and in isolated mitochondria. In addition, oxygen consumption was measured in isolated mitochondria. It was found that curcumin pretreatment attenuates the I/R injury as evidenced by (a) loss of cardiac mechanical work, (b) oxidant stress (increase in lipid peroxidation and decrease in reduced glutathione content) and (c) decrease in the activity of the antioxidant enzymes superoxide dismutase and glutathione reductase in both cardiac tissue and isolated mitochondria, and (d) decrease in mitochondrial respiratory capacity. In conclusion, the protective effect of curcumin was associated with the attenuation of oxidant stress and mitochondrial dysfunction secondary to I/R injury.

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“…Levels of renal glutathione peroxidase activity decreased and those of malondialdehyde increased in cisplatin- induced nephrotoxicity [9]. Witko-Sarsat et al [20] indicated that AOPP accumulation coexists with a decreased glutathione peroxidase level, while the plasma concentration of malondialdehyde remains stable, and this supports the contention that AOPP are more accurate biomarkers of oxidative stress than lipid peroxidation products.…”

mentioning

confidence: 94%

Expressions of Protein Oxidation Markers, Dityrosine and Advanced Oxidation Protein Products in Cisplatin-Induced Nephrotoxicity in Rats

Kimoto

Sugiyama

Nishinohara

et al. 2011

The Journal of Veterinary Medical Science

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ABSTRACT. The purpose of this study was to evaluate whether dityrosine and advanced oxidation protein products (AOPP) reflect the severity of cisplatin-induced nephrotoxicity. Immunoexpression of dityrosine in kidneys and plasma AOPP concentration were examined up to day 4 post-cisplatin injection in rats. Cisplatin injection induced tubular injury on days 2-4 after injection and increased serum creatinine and BUN on days 3 and 4. On days 2-4, dityrosine was immunostained in the cytoplasm of damaged tubular cells, and their immunostaining intensity increased time-dependently. Plasma AOPP levels were significantly increased on days 3 and 4. These results suggest that expressions of dityrosine and AOPP were associated with the severity of renal injury and may be useful markers for the development of cisplatin-induced nephrotoxicity.KEY WORDS: advanced oxidation protein product, cisplatin, dityrosine, nephrotoxicity, oxidative stress.

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Sulforaphane protects against cisplatin-induced nephrotoxicity

Cited by 90 publications

References 24 publications

Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection

Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection

Curcumin Protects from Cardiac Reperfusion Damage by Attenuation of Oxidant Stress and Mitochondrial Dysfunction

Expressions of Protein Oxidation Markers, Dityrosine and Advanced Oxidation Protein Products in Cisplatin-Induced Nephrotoxicity in Rats

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