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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Rotenone exerts similar stimulatory effects on H2O2 production by isolated brain mitochondria from young-adult and old rats

Full text
Author(s):
Michelini, Luiz G. B. [1] ; Figueira, Tiago R. [1] ; Siqueira-Santos, Edilerie S. [1] ; Castilho, Roger F. [1]
Total Authors: 4
Affiliation:
[1] Univ Estadual Campinas, Fac Ciencias Med, Dept Patol Clin, BR-13083887 Campinas, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Neuroscience Letters; v. 589, p. 25-30, MAR 4 2015.
Web of Science Citations: 4
Abstract

Chronic and systemic treatment of rodents with rotenone, a classical inhibitor of mitochondrial respiratory complex I, results in neurochemical, behavioral, and neuropathological features of Parkinson's disease. The aim of the present study was to evaluate whether brain mitochondria from old rats (24 months old) would be more susceptible to rotenone-induced inhibition of oxygen consumption and increased generation of H2O2 than mitochondria from young-adult rats (3-4 months old). Isolated brain mitochondria were incubated in the presence of different rotenone concentrations (5, 10, and 100 nM), and oxygen consumption and H2O2 production were measured during respiratory states 3 (ADP-stimulated respiration) and 4 (resting respiration). Respiratory state 3 and citrate synthase activity were significantly lower in mitochondria from old rats. Mitochondria from young-adult and old rats showed similar sensitivity to rotenone-induced inhibition of oxygen consumption. Similarly, H2O2 production rates by both types of mitochondria were dose-dependently stimulated to the same extent by increasing concentrations of rotenone. We conclude that rotenone exerts similar effects on oxygen consumption and H2O2 production by isolated brain mitochondria from young-adult and old rats. Therefore, aging does not increase the mitochondrial H2O2 generation in response to complex I inhibition. (C) 2015 Elsevier Ireland Ltd. All rights reserved. (AU)

FAPESP's process: 11/50400-0 - Mitochondrial energy metabolism, redox state and functionality in cell death and cardiometabolic and neurodegenerative disorders
Grantee:Aníbal Eugênio Vercesi
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 11/51800-1 - Muscle damage induced by eccentric exercise: involvement of mitochondria and interactions with statin myotoxicity
Grantee:Tiago Rezende Figueira
Support Opportunities: Scholarships in Brazil - Post-Doctoral
FAPESP's process: 11/14229-4 - Mitochondrial generation of reactive oxygen species in the presence of a partial complex I inhibition: Effect of different metabolic states
Grantee:Luiz Guilherme Michelini Bueno
Support Opportunities: Scholarships in Brazil - Master