This study evaluated changes in the antioxidant defences of mitochondria induced by 30 min of forebrain ischemia and recirculation up to 24 h in rats. Following treatment, mitochondria were isolated from two brain subregions: the dorsolateral striatum, an area in which there is loss of most neurons, and the paramedian cortex in which most neurons are resistant to damage. During ischemia and the first few hours of recirculation, the mitochondrial defences were largely preserved based on measurements of the activities of the enzymes, superoxide dismutase, glutathione peroxidase and glutathione reductase, as well as the response of the mitochondria to a subsequent exposure to H2O2 in vitro. However, some moderate changes were detected, particularly in the mitochondria from the dorsolateral striatum. A decrease of 30% in the activity of superoxide dismutase was seen at the conclusion of the ischemic period and a small increase in susceptibility to changes induced by H2O2 was detected during early recirculation. This latter change preceded and possibly contributed to the development of an impairment of respiratory function detected in mitochondria from the dorsolateral striatum at 3 h of recirculation. At 24 h of recirculation, larger changes were seen in the activities of all three of the enzymes in mitochondria from the dorsolateral striatum but not the paramedian cortex that was associated with progression to advanced neuronal damage in the former subregion.
Bibliographical noteFunding Information:
The research described in this paper was supported by the National Health and Medical Research Council (Australia), the Flinders University Research Budget and the Flinders Medical Centre Foundation.
Copyright 2007 Elsevier B.V., All rights reserved.
- Glutathione peroxidase
- Glutathione reductase
- Mitochondrial respiration
- Oxidative damage
- Superoxide dismutase