Antioxidant properties of 2,3,5,7,8-pentahydroxy-6-ethyl-1,4-naphthoquinone (echinochrome A) were linked with the scavenging of peroxy radicals in liposomes, trapping of superoxide anion radicals, and binding of ferrous ions to inactive complexes in the aqueous phase. The antioxidant property of 6-ethyl-2,3,7-trimethoxy-5,8-dihydroxy-1,4-naphthoquinone (trimethoxyechinochrome A) was negligible. Autooxidation of echinochrome A was increased in basic media according to the degree of its dissociation. Autooxidation of polyvalent anions in basic media was accompanied by generation of naphthosemiquinone and superoxide anion radicals as free radical intermediates. An increased rate of echinochrome A autooxidation was noted in the presence of calcium ions. This was explained by a shift of pK of Ca2+-echinochrome A complexes toward acidic pH comparably with echinochrome A. Echinochrome A possessed pronounced mutagenic activity, while trimethoxyechinochrome A was inactive in the Salmonella/mammalian microsome reverse mutation assay (Ames test) for all examined cells (TA98, TA100, TA1537). Comparison of the chemical and biological activity of echinochrome A and trimethoxyechinochrome A demonstrated the key role of the beta-hydroxyl groups in the 2nd, 3rd, and 7th naphthol cycle positions. The O2-* and naphthosemiquinone radicals generated in the redox transition of 2,3-oxygroups may be the reason for the strongly pronounced mutagenicity of echinochrome A.
We studied the state of lysosomal apparatus and pro- and antioxidant activity in the liver of rats with different resistance to hypoxia during postischemic recovery. Under normal conditions the lysosomal apparatus did not differ in highly and low resistant animals. During ischemia and reperfusion the damage to hepatic lysosomal membranes in rats highly resistant to hypoxia was less pronounced than in low resistant animals. These differences also concerned labilization of lysosomes during exposure to damaging factors (hypotonia and Triton X-100). The rats highly resistant to hypoxia differed from low resistant animals by higher stability of lysosomal membranes, lower prooxidant activity (malonic dialdehyde content), and higher tissue concentration of alpha-tocopherol during reperfusion.
Efficacy, safety, and economical aspects of treatment with abacavir, zidovudine, stavudine, and phosphazide in the schemes of antiretroviral therapy of the HIV-infected patients receiving therapy for hepatitis C virus were tested. Clinical, immunological, and virologic efficacy of treatment and dynamics of hemoglobin, thrombocytes, and alanine aminotransferase as markers of common adverse events recorded at the start of the antiviral therapy of chronic hepatitis C and after 4, 8, 12, 24, 48 weeks of the treatment were evaluated. The usage of these drugs in the schemes of antiretroviral therapy exhibited efficacy, high tolerability and safety for all HIV reverse transcriptase inhibitors.
Острые кишечные инфекции остаются одной самых актуальных проблем педиатрии в связи с высоким уровнем заболеваемости, развитием тяжелых форм и летальности, особенно у детей первых пяти лет жизни. В большинстве случаев тяжесть заболевания обусловлена развитием эксикоза, в основе которого лежат потери электролитов и жидкости в следствии эметического и диарейного синдромов. Однако существуют различия в механизмах формирования дегидратации в зависимости от вида инфекционного агента. Так при дегидратации, вызванной вирусами, в основе лежит механизм нарушения абсорбции, причиной которого являются дистрофические изменения в энтероцитах и уменьшение количества клеток, способных адсорбировать жидкость из кишечника. Повышение осмотического давления в процессе нарушенной ферментации нерасщепленных дисахаридов приводит к перемещению воды в просвет кишечника и объясняет появление осмотической диареи и, как следствие, тяжелой дегидратации при отсутствии своевременной коррекции данного патологического состояния. При внедрении бактериальных кишечных патогенов, происходит воздействие различных энтеротоксинов на мембранные комплексы. В частности, стимулируется выработка медиаторов воспаления, повышается уровень внутриклеточного циклического аденозинмонофосфата или циклического гуанозинмонофосфата или происходит нарушение проницаемости слизистой оболочки кишечника под влиянием специфических белков инвазивных патогенов и в целом изменение активности нормального процесса обмена ионов. В статье так же рассмотрены альтернативные механизмы развития диареи при участии энтероэндокринно-нейронных рефлексов, а также описаны типы дегидратации с детализацией водно-электролитных нарушений и современные подходы к регидратационной терапии. Знание и понимание особенностей патогенеза, диагностики типа дегидратации необходимо практикующему врачу для выбора тактики патогенетической терапии острых кишечных инфекций у детей. Acute intestinal infections are one of the most urgent challenges in pediatrics due to a high morbidity, development of severe forms and mortality, especially in children under five years. In most cases, severity of the disease is due to development of exicosis induced by loss of electrolytes and fluids as a result of emetic and diarrheal syndromes. However, the mechanisms of dehydration differ depending on the type of infectious agent. Thus, dehydration caused by viruses is due to the mechanism of absorption disorders induced by dystrophic changes in enterocytes and reduced number of cells that could absorb fluid from the intestine. The increase in osmotic pressure under disturbed fermentation of unsplit disaccharides results in translocation of water into the intestinal lumen, which explains the development of osmotic diarrhea and ensuing severe dehydration in the absence of timely correction of this pathological condition. After invasion of bacterial intestinal pathogens, various enterotoxins impact membrane complexes. Specifically, production of inflammatory mediators is stimulated, levels of intracellular cyclic adenosine monophosphate or cyclic guanosine monophosphate increase, or specific proteins of invading pathogens affect the permeability of intestinal mucosa and, eventually, change the activity of normal ion exchange process. The article also addresses alternative mechanisms of diarrhea involving enteroendocrine-neural reflexes and focuses on types of dehydration with a detailed description of water-electrolyte disorders and modern approaches to rehydration therapy. Knowledge and understanding of the pathogenetic and diagnostic features specific for a dehydration type are necessary for practitioners to choose the tactics for pathogenetic therapy of children’s acute intestinal infections. The aim of this review was to summarize modern aspects of the pathogenesis of exicosis syndrome in acute intestinal infections in young children.
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