Functional State of the Mitochondria from Tissues of the Rat Brain after Chronic Occlusion of the Common Carotid Artery: Role of Lysyl Oxidase
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Stenosis and occlusion of the common carotid artery (CCA) are one of the main reasons of cerebrovascular pathologies; these factors determine the development of hypoperfusion of the brain. Disorders in the expression of lysyl oxidase (LOX) underlie the development of a number of pathological processes, including vascular and cerebral pathologies. Changes in the activity of this enzyme are assumed to significantly affect the functional state of the mitochondria (MCh). We examined the role of LOX in the regulation of energy metabolism in the rat brain under conditions of experimental unilateral chronic occlusion of the CCA (CCA ChO). Experiments were carried out on Wistar rats with ligated left CCA. Animals of one of the experimental groups received drinking water with 0.2% of a LOX blocker, β-aminopropionitrile (BAPN) during 8 weeks. After such course of BAPN introduction, we estimated the characteristics of energy metabolism in the MCh from tissues of the brain hemispheres using a polarographic technique. Occlusion of the CCA was accompanied by disorders in tissue respiration (oxidative phosphorylation in the MCh); these changes were more expressed in the left hemisphere (P < 0.05), but those in the right one were also quite noticeable. There were indications for the existence of interhemisphere differences in the functioning of the MCh complex 1 in healthy control animals; the respective values were greater in the left hemisphere. Introduction of BAPN promoted partial recovery of the MCh functions; this was manifested in some weakening of the effects of CCA occlusion. Thus, under conditions of unilateral CCA ChO, energy metabolism in both brain hemispheres undergoes negative changes. Changes in the LOX activity are one of the factors responsible for negative shifts in the indices of MCh functioning related to hypoperfusion of brain tissues.
Keywordslysyl oxidase (LOX) BAPN (a LOX blocker) brain hypoperfusion mitochondria (MCh) energy metabolism polarography
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