sulforaphane attenuates gentamicin-induced nephrotoxicity: role of mitochondrial protection
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2013
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Abstract
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.
| Reference Key |
negrette-guzmn2013evidence-basedsulforaphane
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| Authors | ;Mario Negrette-Guzmán;Sara Huerta-Yepez;Omar Noel Medina-Campos;Zyanya Lucía Zatarain-Barrón;Rogelio Hernández-Pando;Ismael Torres;Edilia Tapia;José Pedraza-Chaverri |
| Journal | ACS applied materials & interfaces |
| Year | 2013 |
| DOI |
10.1155/2013/135314
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| URL | |
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