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Introduction. One of the pathogenic chains in neurodegenerative diseases, and the Alzheimer’s disease especially, is the disorder of cellular energy supply. Investigation of changes in the indices characterizing a functional state of the mitochondria in the cerebral cortex and hippocampus under the influence of carbacetam, a new modulator of GABA-system, is of a certain interest. The objective of the study was to evaluate the protective effect of carbacetam under conditions of mitochondrial dysfunction of the brain in rats with scopolamine-induced Alzheimer’s disease. Materials and methods. The experiments were conducted on laboratory nonlinear albino male rats with the body weight of 0.18-0.20 kg. To simulate Alzheimer’s disease, scopolamine hydrochloride (Sigma, USA) was injected in rats through the peritoneum, in the dose of 1 mg/kg for 27 days. Since the 28th day of the experiment, carbacetam was introduced through the peritoneum in the dose of 5 mg/kg, in 1 mL of 0.9 % NaCl solution, once a day for 14 days. Results. Under conditions of scopolamine-induced Alzheimer’s disease, light dispersion decreases and a relative rate of mitochondrial swelling increases in the mitochondrial fraction of the cerebral cortex and hippocampus of rats; free radical oxidation of lipids and proteins increases, and activity of Krebs cycle enzymes decreases – -ketoglutarate dehydrogenase and succinate dehydrogenase. After carbacetam administration for 14 days, a gradual decrease of light dispersion and relative rate of mitochondrial swelling are found in the mitochondrial fraction of the cerebral cortex and hippocampus. Moreover, the content of products reacting with 2-thiobarbituric acid and protein oxidation modification in the examined structures decreases; the activity of catalase, -ketoglutarate dehydrogenase, succinate dehydrogenase increases, and superoxide dismutase – only in the cerebral cortex Conclusions. Reduced intensity of mitochondrial swelling, improvement of the antioxidant system state and energy supply of mitochondria in the cerebral cortex and hippocampus of rats with scopolamine-induced Alzheimer’s disease are indicative of mitoprotective properties of carbacetam as a promising neuroprotector.

Introduction. Melatonin, a potent antioxidant agent, is essential for glucose homeostasis. The objective of the study was to determine the influence of melatonin on basal levels of glucose in blood, activities of glucose-6-phosphatase in kidney and liver, pyruvate kinase in muscles and heart, content of glycogen in muscles and heart of rats with alloxan-induced diabetes. Materials and methods. Diabetes was induced in male Wistar rats by single intraperitoneal injection of alloxan monohydrates (170 mg/kg). Four days after diabetes induction, rats were divided into diabetic and melatonin-diabetic groups (10 mg/kg «Sigma» USA, daily and intraperitoneal for 14 days starting from the 5th day). Results. Melatonin injections caused normalization of the elevated serum glucose level in diabetic group of rats compared with basal glucose level before treatment. The activity of pyruvate kinase in muscle and heart tissue of diabetic animals was 45% and 63% less than in control groups, respectively. Regarding kidney and liver of diabetic rats, the activity of glucose-6-phosphatase was increased in average by 148% compared with control value. The glycogen content in the heart and skeleton muscles of diabetic animals was reduced in average by 20% compared with the control. Melatonin restored all these indexes back to normal level. Conclusions. These findings suggested that melatonin restored the events in Cori cycle by possible activation of glycolysis in skeletal and heart muscles and normalization of gluconeogenesis in liver and kidneys.