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Aparicio-Trejo 2018 Free Radic Biol Med

From Bioblast
Publications in the MiPMap
Aparicio-Trejo OE, Reyes-Fermín LM, Briones-Herrera A, Tapia E, León-Contreras JC, Hernández-Pando R, Sánchez-Lozada LG, Pedraza-Chaverri J (2018) Protective effects of N-acetyl-cysteine in mitochondria bioenergetics, oxidative stress, dynamics and S-glutathionylation alterations in acute kidney damage induced by folic acid. Free Radic Biol Med 130:379-96.

» PMID: 30439416 Open Acess

Aparicio-Trejo OE, Reyes-Fermin LM, Briones-Herrera A, Tapia E, Leon-Contreras JC, Hernandez-Pando R, Sanchez-Lozada LG, Pedraza-Chaverri J (2018) Free Radic Biol Med

Abstract: Folic acid (FA)-induced acute kidney injury (AKI) is a widely used model for studies of the renal damage and its progression to chronic state. However, the molecular mechanisms by which FA induces AKI remain poorly understood. Since renal function depends on mitochondrial homeostasis, it has been suggested that mitochondrial alterations contribute to AKI development. Additionally, N-acetyl-cysteine (NAC) can be a protective agent to prevent mitochondrial and renal dysfunction in this model, given its ability to increase mitochondrial glutathione (GSH) and to control the S-glutathionylation levels, a reversible post-translational modification that has emerged as a mechanism able to link mitochondrial energy metabolism and redox homeostasis. However, this hypothesis has not been explored. The present study demonstrates for the first time that, at 24 h, FA induced mitochondrial bioenergetics, redox state, dynamics and mitophagy alterations, which are involved in the mechanisms responsible for the AKI development. On the other hand, NAC preadministration was able to prevent mitochondrial bioenergetics, redox state and dynamics alterations as well as renal damage. The protective effects of NAC on mitochondria and renal function could be related to its observed capacity to preserve the S-glutathionylation process and GSH levels in mitochondria. Taken together, our results support the idea that these mitochondrial processes can be targets for the prevention of the renal damage and its progression in FA-induced AKI model. Keywords: Acute kidney damage, Folic acid, Mitochondrial bioenergetics, Mitochondrial dynamics and S-glutathionylation, N-acetyl-cysteine Bioblast editor: Plangger M O2k-Network Lab: MX Mexico City Pedraza Chaverri J

Labels: MiParea: Respiration, Pharmacology;toxicology  Pathology: Other  Stress:Oxidative stress;RONS  Organism: Rat  Tissue;cell: Kidney  Preparation: Intact cells, Isolated mitochondria  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase 

Coupling state: LEAK, OXPHOS  Pathway: N, S, NS, ROX  HRR: Oxygraph-2k, O2k-Fluorometer 

2018-11, AmR, Safranin