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Wyszukujesz frazę "oxidative damage" wg kryterium: Temat


Tytuł:
Oxidative stress – repair systems of oxidatively damaged biomolecules
Autorzy:
Kołodziej, U.
Maciejczyk, M.
Zalewska, A.
Tematy:
oxidative stress
oxidative damage
oxidative stress repair systems
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Wydawca:
Uniwersytet Medyczny w Białymstoku
Powiązania:
https://bibliotekanauki.pl/articles/1918622.pdf  Link otwiera się w nowym oknie
Opis:
Molecular oxygen (O2), constituting the basis of life on Earth, is classified as a substance with oxidizing properties. Reacting with organic compounds, it leads to their oxidation and at the same time participates in reduction processes. In aerobic organisms, over 90% of oxygen undergoes a total four-electron reduction to produce water molecules (O2 + 4 H+ + 4e- → 2 H2O). The remaining 10% of oxygen, however, is not fully reduced, which results in the production of molecules referred to as reactive oxygen species (ROS). In high concentrations ROS can interact with cellular components (DNA, proteins and lipids), leading to the oxidation of these macromolecules. The resulting oxidation products interfere with the proper functioning of the body by influencing gene expression, intercellular signaling and apoptosis. These changes have been observed in numerous pathological conditions, such as neurodegenerative, cardiovascular, metabolic, autoimmune diseases, and cancer. However, in the context of evolution, living organisms developed specialized repair mechanisms to prevent cellular accumulation of the products of DNA, protein and lipid oxidation, including enzymatic mechanisms (e.g. nucleases, proteases, phospholipases) or removal of damaged DNA, proteins and lipids by apoptosis or autophagy. This article briefly discusses the mechanisms of oxidative modification of cell components and the main repair systems responsible for the removal of lesions in cells by oxidative damage.
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The involvement of oxidative stress in determining the severity and progress of pathological processes in dystrophin-deficient muscles.
Autorzy:
Niebrój-Dobosz, Irena
Hausmanowa-Petrusewicz, Irena
Tematy:
oxidative damage to macromolecules
Duchenne's muscular dystrophy
oxidative stress
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Wydawca:
Polskie Towarzystwo Biochemiczne
Powiązania:
https://bibliotekanauki.pl/articles/1041426.pdf  Link otwiera się w nowym oknie
Opis:
In both forms of muscular dystrophy, the severe Duchenne’s muscular dystrophy (DMD) with lifespan shortened to about 20 years and the milder Becker dystrophy (BDM) with normal lifespan, the gene defect is located at chromosome locus Xp21. The location is the same in the experimental model of DMD in the mdx mice. As the result of the gene defect a protein called dystrophin is either not synthesized, or is produced in traces. Although the structure of this protein is rather well established there are still many controversies about the dystrophin function. The most accepted suggestion supposes that it stabilizes sarcolemma in the course of the contraction-relaxation cycle. Solving the problem of dystrophin function is a prerequisite for introduction of an effective therapy. Among the different factors which might be responsible for the appearance and progress of dystrophic changes in muscles there is an excessive action of oxidative stress. In this review data indicating the influence of oxidative stress on the severity of the pathologic processes in dystrophy are discussed. Several pieces of data indicating the action of oxidative damage to different macromolecules in DMD/BDM are presented. Special attention is devoted to the degree of oxidative damage to muscle proteins, the activity of neuronal nitric oxide synthase (nNOS) and their involvement in defining the severity of the dystrophic processes. It is indicated that the severity of the morbid process is related to the degree of oxidative damage to muscle proteins and the decrease of the nNOS activity in muscles. Estimation of the degree of the destructive action of oxidative stress in muscular dystrophy may be a useful marker facilitating introduction of an effective antioxidant therapy and regulation of nNOS activity.
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Measurements of body temperature and oxidative stress reveal differential costs associated with humoral immune function in a passerine bird
Autorzy:
Zagkle, Elisavet
Bryła, Amadeusz
Bauchinger, Ulf
Sadowska, Edyta
Cichoń, Mariusz
Opis:
Eco-immunology considers resistance to antigens a costly trait for an organism, but actual quantification of such costs is not straightforward. Costs of the immune response are visible in impaired coloration and reduced growth or reproductive success. Activation of the humoral immune response is a slow, complex and long-lasting process, which makes the quantification of its energetic cost a potential losing game. We implemented near-continuous measurements of body temperature in zebra finches (Taeniopygia guttata) as a proxy for the energetic cost, with a particular focus during activation of the humoral immune response until the peak of antibody release several days later. At the peak of the antibody release we additionally measured oxygen consumption (open-flow respirometry) and markers of oxidative stress (dROMs, OXY). Birds with an activated immune response maintained a higher night-time body temperature during the first 4 nights after an immune challenge in comparison to controls, implying increased night-time energy use. At peak antibody production, we did not find differences in night-time body temperature and oxygen consumption but observed differentiated results for oxygen consumption during the day. Immune-challenged females had significantly higher oxygen consumption compared with other groups. Moreover, we found that activation of the humoral immune response increases oxidative damage, a potential cost of maintaining the higher night-time body temperature that is crucial at the early stage of the immune response. The costs generated by the immune system appear to consist of two components - energetic and non-energetic - and these appear to be separated in time.
Dostawca treści:
Repozytorium Uniwersytetu Jagiellońskiego
Artykuł
Tytuł:
Assessment of DNA damage profile and oxidative /antioxidative biomarker level in patients with inflammatory bowel disease
Autorzy:
Mrowicka, Małgorzata
Mrowicki, Jerzy
Mik, Michał
Dziki, Łukasz
Dziki, Adam
Majsterek, Ireneusz
Tematy:
DNA oxidative damage repair
inflammatory bowel diseases
pro/antioxidant status
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Wydawca:
Index Copernicus International
Powiązania:
https://bibliotekanauki.pl/articles/1391884.pdf  Link otwiera się w nowym oknie
Opis:
Aim: The purpose of this study was to investigate the oxidative DNA damage, pro-antioxidant status in Polish patients with inflammatory bowel disease (IBD). Methods: Oxidative DNA damage was measured by comet assay techniques; nitric oxide (NO) and plasmatic lipid peroxidation (MDA) as oxidative stress were valuated by colometric methods; superoxide dismutase (SOD1), catalase (CAT) and glutathione peroxidase (GPx1) as antioxidative defense were determined by spectrophotometric methods. Results: The level of oxidative DNA damage in IBD patients was significantly higher in relation to controls (P = 0.01). Alike, in control subject as well as in patients with IBD, lymphocytes are characterized by complete repair of DNA damage. A significant decrease of SOD (P = 0.031), CAT (P = 0.006), GPx1 (P = 0.001) activity was seen in IBD patients vs control. MDA (P = 0.001) and NO (P = 0.001) concentrations were significantly increased in IBD patients as compared to healthy subjects. Conclusions: Our results may be due to the induction of DNA repair genes which may occur at the stage of the pathological changes (IBD) that may be caused by excessive oxidative stress. However, the cause of this relationship, and whether it is direct or indirect, remains to be explored.
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Impact of the Ser326Cys polymorphism of the OGG1 gene on the level of oxidative DNA damage in patients with colorectal cancer
Autorzy:
Kabzinski, Jacek
Walczak, Anna
Dziki, Adam
Mik, Michał
Majsterek, Ireneusz
Tematy:
colorectal cancer
OGG1
8-oxoguanine
DNA repair
oxidative damage
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Wydawca:
Index Copernicus International
Powiązania:
https://bibliotekanauki.pl/articles/1392877.pdf  Link otwiera się w nowym oknie
Opis:
As a result of reactive oxygen species operation, cell damage occurs in both cellular organelles and molecules, including DNA. Oxidative damage within the genetic material can lead to accumulation of mutations and consequently to cancer transformation. OGG1 glycosylase, a component of the Base Excision Repair (BER) system, is one of the enzymes that prevents excessive accumulation of 8-oxoguanine (8-oxG), the most common compound formed by oxidative DNA damage. In case of structural changes of OGG1 resulting from polymorphic variants, we can observe a significant increase in the concentration of 8-oxG. Linking individual polymorphisms to DNA repair systems with increased risk of colorectal cancer will allow patients to be classified as high risk and included in a prophylactic program. The aim of the study was to determine the level of oxidative DNA damage and to analyze the distribution of Ser326Cys polymorphism of the OGG1 gene in a group of patients with colorectal cancer and in a control group in the Polish population. Material and methodology. DNA was isolated from the blood of 174 patients with colorectal cancer. The control group consisted of 176 healthy individuals. The level of oxidative damage was determined by analyzing the amount of 8-oxguanine using the HT 8-oxo-dG ELISA II Kit. Genotyping was performed via the TaqMan method. Results. The obtained results indicate that Ser326Cys polymorphism of the OGG1 gene increases the risk of RJG and is associated with significantly increased levels of 8-oxoguanine. Conclusions. Based on the results obtained, we conclude that Ser326Cys polymorphism of the OGG1 gene may modulate the risk of colorectal cancer by increasing the level of oxidative DNA damage.
Dostawca treści:
Biblioteka Nauki
Artykuł

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