title: [DYNAMICS OF GLUTAMINE SYNTHASE ACTIVITY IN RAT BRAIN IN PRENATAL HYPOXIA MODEL].
abstract: Prenatal ontogenesis is a period of high sensitivity to stressful impact, so any stressor can lead to changes of physiological, biochemical indicators, behavioral and cognitive functions. The most common and clinically significant stress factor, which the embryo may be exposed during embryonic development, is hypoxia. In this case pathological changes in the central nervous system depend on the duration and severity of hypoxic exposure, individual tolerance and the stage of prenatal development, at each of which in the brain take place the basic histogenetic processes. By activating energetically disadvantageous anaerobic glycolysis hypoxia leads to excess of glutamate emission and cell apoptosis. Glutamine synthase is a basic enzyme that regulates metabolism of glutamate, catalyzing conversion of glutamate to glutamine with ammonia detoxification. The aim of the presented work was to reveal changes in the activity of one of the key enzyme of glutamate metabolism- glutamine synthetase in the brain of offspring of white rats undergone to hypoxia at different stages of prenatal ontogenesis. Hypoxia was created by placing female rats at stages of the pregnancy, corresponding to progestation period of organogenesis and fetal period of prenatal development, in the hypobaric chamber with exposure to 5% oxygen and 95% nitrogen gas mixture during 30 minutes per day. The offspring obtained from females of control and experimental groups were used for biochemical determinations in the age of 1 and 3 month. It has been established that hypoxia exposed to pregnant females during embryonic organogenesis causes significant changes in enzyme activity, particularly pronounced in the cerebral cortex and cerebellum, as compared with progestational and fetal hypoxia. Enzyme activity decreased in a greater degree in one-month-old rats undergone to prenatal hypoxia, than three- month-old animals. Thus, stress during intensive processes of proliferation and migration of cells of the forming brain violates glutamate metabolism of the brain.
authors: V R
authors: VR
authors: Khairova
authors: M I
authors: MI
authors: Safarov
mesh_terms: D000641:Ammonia / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001923:Brain Chemistry; D002531:Cerebellum / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development; D002540:Cerebral Cortex / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development; D004622:Embryo, Mammalian; D005260:Female; D018507:Gene Expression Regulation, Developmental; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism*; D005973:Glutamine / Q000378:metabolism*; D007031:Hypothalamus / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development; D000860:Hypoxia / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D018811:Maternal Exposure; D008526:Medulla Oblongata / Q000187:drug effects / Q000201:enzymology / Q000254:growth & development; D038081:Organogenesis / Q000187:drug effects / Q000235:genetics; D010100:Oxygen / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological
chemical_list: D005973:Glutamine; D018698:Glutamic Acid; D000641:Ammonia; D005974:Glutamate-Ammonia Ligase; D010100:Oxygen