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The effect of α2-adrenoblocker mesedin (2-(2-methylamino-4-thiazolyl)-1,4-benzodioxane hydrochloride) on the content of oxidative stress biomarkers in the brain tissue was well studied in ischemic disorders. The aim of this study is to reveal the possible mechanisms of the antihypoxic effect of mesedin. The quantitative changes of the final product of lipid peroxidation (LP)—malondialdehyde (MDA) and carbonyl derivatives of proteins — aldehyde-dinitrophenylhydrazones of neutral character (ADNPuv), ketone-dinitro-phenylhydrazones of neutral character (KDNPuv), aldehyde-dinitrophenylhydrazones of basic character (ADNPvs) and ketone-dinitrophenylhydrazones of basic character (KDNPvs) were studied in the brain tissue of rats (n = 56) under the condition of experimental ischemia caused by the ligation of the right common carotid artery. The study showed that one of the possible mechanisms of antihypoxic action of mesedin is its ability to prevent the accumulation of malondialdehyde and to limit protein carbonylation in brain ischemia. The data received demonstrates that mesedin could serve as a potential medicine for the correction of cerebrovascular ischemic disorders, for the reason that along with improving cerebral blood flow and preventing the development of morphological shifts and neurobehavioral disturbances in brain local ischemia, the medicine also mitigates the aggressive action of oxidative stress while protecting the brain tissue from the consequences of hypoxia.

The level of expression of transcription factor genes (GATA-3, TBX21, IL23A), and changing of oxidative modification of proteins in young and elderly healthy persons was studied. The results of evaluation of gene expression, GATA-3 in lymphocytes showed the increased expression of GATA-3 in elderly people in comparison with the young. Women demonstrated higher expression of GATA-3 in compare with men. Study of IL-2p showed reduced levels of expression in aged humans compared to young. TVH21 expression level showed a reduction expression in both men and women. Comparative analysis of protein oxidation in blood plasma of young and elderly people showed an increase in the intensity of oxidative modification of proteins in the elderly.Проведено исследование уровня экспрессии генов транскрипционных факторов (GATA-3, TBX21, IL23A), а также изменения окислительной модификации белков у молодых, и пожилых здоровых людей. Результаты оценки экспрессии генов, GATA-3 в лимфоцитах показал, что у пожилых людей наблюдается увеличение экспрессии GATA-3 по сравнению с молодыми. При сравнении показателей экспрессии у мужчин и женщин обнаружено, что у женщин экспрессия GATA-3 выше, чем у мужчин. Исследование гена IL23A обнаружило снижение уровня экспрессии у пожилых людей по сравнению с молодыми. Уровень экспрессии ТВХ21 показал также уменьшение экспрессии как у мужчин, так и у женщин. Сравнительный анализ окисления белков в плазме крови у молодых и пожилых людей выявил повышение интенсивности окислительной модификации белков у пожилых людей.

A blood cytokine profile and also the brain content of lipid peroxidation (LPO) products and gangliosides were investigated in rats with experimental brain edema. The development of brain edema was accompanied by the increase in pro-inflammatory and a decrease in anti-inflammatory cytokine content. In parallel, accumulation of LPO products (conjugated dienes, hydroperoxides, and malondialdehyde) was observed. The study of ganglioside content under conditions of experimental brain edema revealed a decrease of their hydrolytic degradation product, sphingosine.

The content of cytokines, and gangliosides metabolism, and the quantity of lipid peroxidation products were studied at experimental brain edema. Data obtained show increase the level of proinflammatory cytokins and decrease the level of antiinflammatory cytokines during development of brain edema. Along with this we reveal the accumulation of lipid peroxidation products (diene conjugates, hydroperoxides, and malonic dialdehyde). Each fraction of gangliosides decreased, but the product of their hydrolytic dissociation sphingosine increased at experimental brain edema.

To investigate the free radical oxidation of lipids, oxidative modification of protein activity of glutathione peroxidase and glutathione reductase as well as the end product of nitric oxide - nitrite in the brain mitochondrial fraction of animals with experimentally induced cerebral edema and in treatment with taurine.Toxic brain edema was induced in rats with intraperitoneal injection of tetra-ethyl lead (10 mg per kg of animal weight). The intensity of peroxidation was evaluated by hydroperoxide and malonic aldehyde contents.An analysis of the levels of oxidative modification of proteins revealed that brain edema was characterized by increased levels of oxidative modification of proteins and lipids, nitrogen oxide, reduced glutathione content and decrease in the activity of enzymes containing glutathione (glutathione peroxidase and glutathione reductase).On this basis, we suggested that drugs increasing glutathione content and activating enzymes containing glutathione, for example taurine, could be used as medications. The introduction of taurine in dose of 50 mg/kg during 5 days led to the reduction of lipid peroxidation products, normalization of oxidative modification of proteins in the mitochondrial fraction of the rats with experimental cerebral edema.Цель исследования - изучение свободнорадикального окисления липидов, окислительной модификации белка, активности глутатионпероксидазы и глутатионредуктазы, а также конечного продукта оксида азота - нитрита в митохондриальной фракции головного мозга животных во время экспериментально вызванного отека мозга при лечении таурином. Материал и методы. Токсический отек головного мозга вызывали внутрибрюшинным введением крысам тетраэтилолова в дозе 10 мг на 1 кг массы животного. Интенсивность перекисного окисления липидов регистрировали по содержанию гидроперекисей и малонового диальдегида. Результаты и заключение. Анализ уровней окислительной модификации белков показал, что отек мозга характеризуется повышением содержания продуктов окислительной модификации белков и липидов, оксида азота, а также снижением содержания глутатиона и понижением активности глутатионсодержащих ферментов (глутатионпероксидаза и глутатионредуктаза). Исходя из этого, большой интерес вызывает использование препаратов, которые могут повышать содержание глутатиона и активизировать ферменты, содержащие его в своей структуре. К таким препаратам относится таурин. По нашим данным, введение таурина в течение 5 дней в дозе 50 мг/кг приводило к уменьшению содержания продуктов перекисного окисления липидов, нормализации окислительной модификации белков в митохондриальной фракции головного мозга крыс с экспериментальным отеком мозга.

BACKGROUND: Familial Mediterranean fever (FMF) is a genetically linked disorder common amongst races of the Eastern Mediterranean region. Typical symptoms include episodic pain syndrome extending throughout the chest or abdomen associated with histopathological signs of amyloidosis of the kidney. AIM: To investigate possible connections between the aseptic inflammation that occurs during pain crises and cell membrane structural and functional integrity in patients with FMF. METHODS: Oxidative stress parameters in 42 patients in remission and during a pain crisis were compared with 21 normal subjects. RESULTS: The patient group had significantly greater concentrations of chemiluminescent and thiobarbituric acid-reactive substances in the blood plasma and lower concentrations of alpha-tocopherol than the control group while in remission; these changes were exacerbated during pain crises. Analyses of the phospholipid composition of erythrocyte membranes showed significant increases in amounts of acidic phospholipids (phosphatidic acid, monophosphatidylinositol and cardiolipin) and lysophosphatidylcholine compared with healthy subjects. CONCLUSIONS: The pattern of differences in membrane phospholipid composition was consistent with increased oxidative stress in patients with FMF.

SummaryRat brain slices have been incubated in the presence of watersoluble synthetic peptide fragments corresponding to residues 1-9 and 1-15 of the N-terminus of immunophilin and the effects on the phospholipid composition examined. During a 2h incubation in the presence of 1 nm, 0-1 μM and 10μM concentrations of the peptides there were significant and dose-dependent decreases in the amounts of phosphatidylcholine and phosphatidylethanolamine and increases in the amounts of phosphatidylserine and, to a lesser extent, phosphatidyl-inositol, cardiolipin and lysophosphatidylcholine. The overall decrease in the neutral phospholipids and increase in the acidic phospholipids tended to counteract any change in the phospholipid composition of the tissue. The results are discussed in terms of the possible effects of immunophilin on modulating phospholipid turnover in brain cell membranes.