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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 135314, 17 pages
Research Article

Sulforaphane Attenuates Gentamicin-Induced Nephrotoxicity: Role of Mitochondrial Protection

1Departamento de Biología, Facultad de Química, UNAM, 04510 Mexico City, DF, Mexico
2Unidad de Investigación en Enfermedades Oncológicas, Hospital Infantil de México “Federico Gómez”, 06720 Mexico City, DF, Mexico
3Sección de Patología Experimental, Instituto Nacional de Ciencias Médicas y Nutrición “Salvador Zubirán”, 14000 Mexico City, DF, Mexico
4Unidad del Bioterio, Facultad de Medicina, UNAM, 04510 Mexico City, DF, Mexico
5Laboratorio de Fisiopatología Renal, Departamento de Nefrología, Instituto Nacional de Cardiología “Ignacio Chávez”, 14080 Mexico City, DF, Mexico

Received 18 December 2012; Revised 16 February 2013; Accepted 19 February 2013

Academic Editor: José Luis Ríos

Copyright © 2013 Mario Negrette-Guzmán et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.