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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 940627, 10 pages
Research Article

Increased Susceptibility of Gracilinanus microtarsus Liver Mitochondria to Ca2+-Induced Permeability Transition Is Associated with a More Oxidized State of NAD(P)

1Department of Clinical Pathology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), 13087-877 Campinas, SP, Brazil
2Graduate Program in Ecology, Biology Institute, State University of Campinas, 13087-877 Campinas, SP, Brazil
3Department of Animal Biology, Biology Institute, State University of Campinas, 13087-877 Campinas, SP, Brazil

Received 7 April 2015; Revised 22 May 2015; Accepted 27 May 2015

Academic Editor: Andrés Trostchansky

Copyright © 2015 Juliana A. Ronchi 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.


In addition to be the cell’s powerhouse, mitochondria also contain a cell death machinery that includes highly regulated processes such as the membrane permeability transition pore (PTP) and reactive oxygen species (ROS) production. In this context, the results presented here provide evidence that liver mitochondria isolated from Gracilinanus microtarsus, a small and short life span (one year) marsupial, when compared to mice, are much more susceptible to PTP opening in association with a poor NADPH dependent antioxidant capacity. Liver mitochondria isolated from the marsupial are well coupled and take up but exhibited a much lower retention capacity than mouse mitochondria. Although the known PTP inhibitors cyclosporin A, ADP, and ATP significantly increased the marsupial mitochondria capacity to retain , their effects were much larger in mice than in marsupial mitochondria. Both fluorescence and HPLC analysis of mitochondrial nicotinamide nucleotides showed that both content and state of reduction (mainly of NADPH) were lower in the marsupial mitochondria than in mice mitochondria despite the similarity in the activity of the glutathione peroxidase/reductase system. Overall, these data suggest that PTP opening is an important event in processes of signalling to cell death mediated by mitochondrial redox imbalance in G. microtarsus.