Effect of coenzyme Q(10) on biochemical and morphological changes in experimental ischemia in the rat brain

• Published in: Brain research bulletin Vol. 53; no. 4; p. 399
• Main Author: Ostrowski, R P
• Format: Journal Article
• Language: English
• Published: United States 01.11.2000
• Subjects: Adenosine Triphosphate - metabolism; Animals; Brain - drug effects; Brain - metabolism; Brain - pathology; Brain Ischemia - chemically induced; Brain Ischemia - metabolism; Brain Ischemia - pathology; Brain Stem - metabolism; Cerebellum - metabolism; Cerebral Cortex - metabolism; Cerebral Ventricles - drug effects; Cerebral Ventricles - physiology; Coenzymes; Disease Models, Animal; Endothelin-1 - administration & dosage; Endothelin-1 - pharmacology; Functional Laterality; Glutathione - metabolism; Glutathione Disulfide - metabolism; Hippocampus - drug effects; Hippocampus - metabolism; Injections, Intraventricular; Lactates - metabolism; Male; Neurons - drug effects; Neurons - metabolism; Neurons - pathology; Pyramidal Cells - drug effects; Pyramidal Cells - metabolism; Rats; Rats, Wistar; Superoxide Dismutase - metabolism; Ubiquinone - administration & dosage; Ubiquinone - analogs & derivatives; Ubiquinone - pharmacology
• ISSN: 0361-9230
• DOI: 10.1016/S0361-9230(00)00406-8

The aim of the work was to evaluate an influence of CoQ(10) on lactate acidosis, adenosine-5'-triphosphate (ATP) concentrations, oxidized to reduced glutathione ratio and on superoxide dismutase activity in endothelin model of cerebral ischemia in the rat. Light microscopic studies in the central nervous system and morphometric analysis of pyramidal cells in the hippocampus were also performed. Endothelins (ET-1 or ET-3; 20 pmoles) were injected into the right lateral cerebral ventricle (intracerebroventricularly). CoQ(10) was given intraperitoneally (i.p.) just before the operation (i.p. 10 mgkg b. wt.). More severe changes of investigated biochemical parameters were observed in the animals treated with ET-1 in comparison with ET-3. Recovery was noted earlier in the group subjected to ET-3 and CoQ(10) administration, than in the animals subjected to ET-1 and CoQ(10) treatment. Histopathological observations showed sparse foci of a neuronal loss in the cerebral cortex and in the hippocampus only in the ET-1 model of ischemia. Additionally more numerous dark neurons were present in above brain structures following ET-1 administration comparing with ET-3 one. Morphometrical studies demonstrated that CoQ(10) diminished neuronal injury in the hippocampal CA1, CA2 and CA3 zones. Above data indicate on neuroprotective effect of CoQ(10) as a potent antioxidant and oxygen derived free radicals scavenger in the cerebral ischemia.