title: [Contribution and role of important biochemic factors in cerebral ischemia].
abstract: After an ischemic insult, a multi-faceted complex cascade of biochemical reactions occurs that ultimately causes neurons death. Above reactions exert an influence on: immunological changes (activation of the complement system and the generation of antibodies), increased inflammation (actions of proinflammatory cytokines and chemokines), the production of reactive oxygen species leading to oxidative stress, diminished mitochondrial function and activation of apoptotic pathways. There is also intensive release and wrong reversible escapement many of neurotransmitters. The last one throught oxidative desamination are one of the main sources most of free radicals. Central nervous system is particularly susceptible to ROS-induced damage due to the high oxygen demands of the brain and low concentration of endogenous antioxidants. lts refer both enzymatic antioxidants: catalase, glutathione peroxidase, glutathione reductase, superoxide dismutase and nonenzymatic antioxidants glutathione, vitamin a, c, e, coenzym Q, uric acid etc. Presently there are no neuroprotective treatments and prevention. One way of treatment testing in clinical trials is hypothermia inhibits above-mentioned processes.
authors.affiliation: III Miejski Szpital w Lodzi, Oddział Rehabilitacji.
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Miller
authors.forename: Maciej
authors.initials: M
authors.lastname: Rutkowski
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002545:Brain Ischemia / Q000503:physiopathology* / Q000628:therapy; D003165:Complement System Proteins / Q000276:immunology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D018384:Oxidative Stress / Q000276:immunology
chemical_list: D000975:Antioxidants; D018836:Inflammation Mediators; D003165:Complement System Proteins