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1
100%
EN
Besides the structural function in proteins, aromatic amino acids are precursors of many important biological compounds essential for normal functioning of the human organism. Many of these compounds may be used as markers for identification of specific pathological states. Comprehensive knowledge about the metabolism of aromatic amino acids and mechanisms of action of their metabolites made it possible to develop effective treatments for many disorders. However, it should not be forgotten that in some pathological conditions, these compounds could not only be involved in the pathogenesis of many disease entities but could also be used as an important tool in prediction of many diseases. This paper contains a review of published literature on aromatic amino acids in the context of physiological processes of the human body and chosen social disorders, such as cancers; psychiatric disorders: depression, anxiety states, schizophrenia, bipolar affective disorders; neurodegenerative, and cardiovascular diseases; chronic kidney insufficiency or diabetes.
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2014
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vol. 61
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issue 4
795-799
EN
The protective action of quercetin against the pro-oxidant and apoptotic effect of etoposide was investigated in HL-60 cells with a high level of myeloperoxidase (MPO) activity and in cells treated with MPO inhibitor, 4-aminobenzoic acid hydrazide (ABAH). Quercetin significantly protected MPO-rich cells against the pro-oxidative (p<0.05) and apoptotic (p<0.05) effects of etoposide. Pre-treatment with ABAH abolished this protective influence of quercetin on apoptosis induced by etoposide but actually enhanced the action effect of quercetin against etoposide-generated reactive oxygen species (ROS) level by this cytostatic drug. Thus quercetin can protect HL-60 cells against the pro-oxidative activity of etoposide regardless of MPO activity.
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2011
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vol. 58
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issue 1
89-94
EN
Despite numerous theories, the etiology and pathogenesis of primary varicose veins remain unclear. The etiology of chronic venous diseases (CVDs) known as chronic venous insufficiency (CVI) is related to leukocyte trapping. Leukocyte trapping involves trapping of white cells in vessel walls followed by their activation and translocation outside the vessel. Release of reactive oxygen species (ROS) from trapped white cells has been documented. Superoxide dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as malonyldialdehyde (MDA). The aim of this study was to determine the involvement of free radicals in the etiology of venous changes. The following material was used for the study: fragments of sufficient or insufficient venous system and varices from 31 patients diagnosed with chronic venous disease in the 2nd or 3rd degree, according to clinical state, etiology, anatomy and pathophysiology (CEAP), which were qualified for surgical procedure. The levels of oxidative stress markers strongly correlated with lesions observed by USG in insufficient and varicose veins. In both a higher concentration of MDA was observed, which is a sign of lipid peroxidation. Antioxidative mechanisms, SOD activity and total antioxidative power expressed as FRAP were inversely proportional to MDA concentration. In insufficient and varicose veins both FRAP and SOD activities were significantly lower than in normal veins. The severity of clinical changes was inversely dependent on the efficiency of scavenging of ROS, which additionally proves the participation of free radicals in pathogenesis of CVDs.
4
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Salivary proteins in health and disease

51%
EN
Besides their structural catalytic and diverse regulatory functions, proteins are also precursors of many important biological compounds essential for normal functioning of humans. Many of these compounds may be used as markers for identification of specific pathological states. A comprehensive knowledge about the metabolism of salivary proteins and the mechanisms of action of their metabolites allowed the development of effective treatment for many disorders. However, it should not be forgotten that in some pathological conditions, these compounds not only could be involved in the pathogenesis but also could be used as tool in the prediction of many diseases. This paper is a review of the published literature on selected salivary proteins in the context of the physiological processes of the human body and chosen chronic disorders, such as diabetes, diabetic nephropathy, mucositis, oral mycoses and caries.
EN
Schizophrenia is a very serious and growing medical and social problem. Despite advances in pharmacotherapy and other forms of psychosis therapy, schizophrenia remains a chronic and degrading disorder. Several decades of research on the determinants of schizophrenia brought no insight into its aetiology. Hypotheses confirmed in the studies and verified in clinical practice either fail to account for the causes of schizophrenia or explain only some of its manifestations. The well-known and widely described models of impaired dopaminergic (the dopamine hypothesis) or serotonergic neurotransmission, which provide foundations for the contemporary pharmacotherapy, may serve as an example. However, such an intervention does not interfere with the mechanisms underlying the disease, but only eliminates some of the symptoms, with no effects on cognitive deficits. Studies on risk factors for schizophrenia, its first episode in particular, increasingly emphasise the importance of interactions between immunological dysregulation, oxidant-antioxidant imbalance, disturbances of the intestinal barrier and epigenetic phenomena. This fact points to the need to modify the classical metaconcept of the development of schizophrenia by adding the aspect of interaction between a range of diverse biological and psychosocial phenomena. There are many individual observations in the subject literature, however, studies exploring the relationships between immunological and inflammatory phenomena, gene expression and the dynamics of changes in the clinical condition in the course of treatment are lacking. The presented etiopathogenetic mechanisms of the disease are a potential goal of future research strategies, which may additionally reinforce both the more personalised approach and the potential of combined therapies.
PL
Schizofrenia należy do coraz poważniejszych problemów medycznych i społecznych. Pomimo postępu w farmakoterapii i innych formach terapii psychoz pozostaje ona zaburzeniem o chronicznym i degradującym przebiegu. Kilka dekad badań nad jej uwarunkowaniami nie przyniosło odkrycia etiologii choroby. Potwierdzone w badaniach i zweryfikowane w praktyce klinicznej hipotezy nie tłumaczą przyczyn jej powstawania lub ograniczają się do wyjaśnienia tylko części manifestowanych objawów. Przykładem mogą być szeroko znane i opisane modele zaburzenia neurotransmisji dopaminergicznej (teoria dopaminowa) czy serotoninergicznej, na których opiera się współczesna farmakoterapia. Jest to jednak interwencja nie ingerująca w mechanizmy powstawania choroby, lecz tylko usuwająca część objawów, bez wpływu na deficyty poznawcze. Coraz częściej w badaniach nad czynnikami ryzyka schizofrenii – w tym zwłaszcza jej pierwszego epizodu – podnosi się znaczenie interakcji między dysregulacją immunologiczną, zaburzeniami równowagi oksydacyjno-antyoksydacyjnej, zakłóceniami bariery jelitowej oraz zjawiskami o charakterze epigenetycznym. Fakt ten wskazuje na konieczność zmodyfikowania klasycznych metakoncepcji nt. rozwoju schizofrenii o wymiar oddziaływania pomiędzy szeregiem różnorodnych zjawisk biologicznych a zjawiskami psychospołecznymi. W literaturze przedmiotu znaleźć można wiele pojedynczych obserwacji, brakuje jednak przekrojowych badań, w których sprawdzano by zależności między zjawiskami immunologicznymi i zapalnymi, ekspresją genów a dynamiką zmian stanu klinicznego w przebiegu leczenia. Przedstawione w tekście mechanizmy etiopatogenezy choroby stanowią potencjalny cel przyszłych strategii badawczych, które dodatkowo powinny wzmacniać podejście spersonalizowane i potencjał terapii skojarzonych.
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