Journal
TOXICOLOGY LETTERS
Volume 199, Issue 1, Pages 80-92Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2010.08.009
Keywords
Cisplatin; Sulforaphane; Mitochondrial alterations; Nephrotoxicity; NAD(P)H: quinone oxidoreductase 1; gamma Glutamyl cysteine ligase
Categories
Funding
- National Council of Science and Technology (CONACYT), Mexico [80791, 129838]
- Direccion General de Asuntos del Personal Academico, UNAM [PAPIIT IN201910]
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This work was designed to further study the mechanism by which sulforaphane (SFN) exerts a reno-protective effect against cisplatin (CIS)-induced damage. It was evaluated whether SFN attenuates the CIS-induced mitochondrial alterations and the impairment in the activity of the cytoprotective enzymes NAD(P)H: quinone oxidoreductase 1 (NQO1) and gamma glutamyl cysteine ligase (gamma GCL). Studies were performed in renal epithelial LLC-PK1 cells and in isolated renal mitochondria from CIS, SFN or CIS + SFN treated rats. SFN effectively prevented the CIS-induced increase in reactive oxygen species (ROS) production and the decrease in NQO1 and gamma GCL activities and in glutathione (GSH) content. The protective effect of SFN on ROS production and cell viability was prevented by buthionine sulfoximine (BSO), an inhibitor of gamma GCL, and by dicoumarol, an inhibitor of NQO1. SFN was also able to prevent the CIS-induced mitochondrial alterations both in LLC-PK1 cells (loss of membrane potential) and in isolated mitochondria (inhibition of mitochondrial calcium uptake, release of cytochrome c, and decrease in GSH content, aconitase activity, adenosine triphosphate (ATP) content and oxygen consumption). It is concluded that the protection exerted by SFN on mitochondrial alterations and NQO1 and gamma GCL enzymes may be involved in the renoprotection of SFN against CIS. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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