Wyniki wyszukiwania - Biblioteka Nauki

1

Oxidative stress – repair systems of oxidatively damaged biomolecules

100%

Kołodziej U. , Maciejczyk M. , Zalewska A.

Progress in Health Sciences

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2018

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tom 8(1)

141-150

EN

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.

2

Impact of the Ser326Cys polymorphism of the OGG1 gene on the level of oxidative DNA damage in patients with colorectal cancer

88%

Kabzinski J. , Walczak A. , Dziki A. , Mik M. , Majsterek I.

Polish Journal of Surgery

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2018

|

tom 90(2)

13-15

EN

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.

3

Histopathological changes and oxidative damage in hepatic tissue of rats experimentally infected with Babesia bigemina

75%

Esmaeilnejad B. , Tavassoli M. , Samiei A. , Abbasi A. , Shafipour A. , Esmaeilnejad N.

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tom 21

|

nr 3

4

Whether ferredoxin-dependent cyclic electron transport (CET) limits ROS production in Thelungiella salsuginea?

63%

Wiciarz M. , Pilarska M. , Kruk J. , Niewiadomska E.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

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nr 2

5

The changes in non enzymatic antioxidants in halophyte Cakile maritima under arsenic and salt stress

63%

Demir E. , Seckin Dinler B. , Ozdener Y.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

|

nr 2

6

Stres oksydacyjny i wewnątrzkomórkowe mechanizmy antyoksydacyjne

63%

Cal M. , Kilisch J.

Laboratorium - Przegląd Ogólnopolski

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2020

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tom nr 1

38--43

PL

Wszystkie organizmy żywe są narażone na działanie czynników zewnętrznych, które mogą indukować stres komórkowy. Wolne rodniki, których poziom jest kontrolowany przez mechanizmy wewnątrzkomórkowe, są niezbędne dla prawidłowego funkcjonowania komórki. Nadmiar wolnych rodników prowadzi do stresu oksydacyjnego. W komórkach w odpowiedzi na stres oksydacyjny są uruchamiane procesy mające na celu neutralizację nadmiaru wolnych rodników, aby zapobiec ich szkodliwemu wpływowi na elementy składowe komórki. W wyniku stresu oksydacyjnego uszkodzeniu mogą ulec tak ważne elementy komórki jak materiał genetyczny czy lipidy i białka. Bardzo ważną rolę w walce z wolnymi rodnikami odgrywają antyoksydanty, które są produkowane wewnątrzkomórkowo oraz te, które dostępne są jako suplementy diety lub po prostu w żywności.

EN

All living organisms are exposed to external factors that can induce cellular stress. Free radicals, whose level is controlled by intracellular mechanisms, are necessary for the proper functioning of a cell. Excess free radicals lead to oxidative stress. In cells, in response to oxidative stress, processes are initiated to neutralize excess free radicals in order to prevent their harmful effects on the cell's components. As a result of oxidative stress, such important elements of the cell as genetic material, lipids and proteins may be damaged. Antioxidants that are produced intracellularly and those that are available as dietary supplements or simply in food play a very important role in the fight against free radicals.

7

Lipid peroxidation and photosynthetic apparatus oxidative damage in two varieties of grapevine growing in Mediterranean climate

63%

Dinis L. , Malheiro A. , Santos D. , Ferreira H. , Bacelar E. , Goncalves B. , Moutinho-Pereira J. , Correia C.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

|

nr 2

8

Assessment of the antioxidant effectiveness of alpha-lipoic acid in healthy men exposed to muscle-damaging exercise

63%

Zembron-Lacny A. , Slowinska-Lisowska M. , Szygula Z. , Witkowski K. , Stefaniak T. , Dziubek W.

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tom 60

|

nr 2

139-143

EN

The aim of this study was to compare the indices of glutathione antioxidant system and oxidative damage level in resistance trained and untrained subjects and to assess the antioxidant action of -lipoic acid in trained men exposed to muscle-damaging exercise. Thirteen trained and twenty untrained men (NT) participated in the comparative study. Then trained men were randomly assigned to TCON group (control) or TALA group (-lipoic acid, 600 mg . day-1, for 8 days) and performed isometric/isokinetic effort of quadriceps muscles. The study has shown the significantly higher erythrocyte levels of glutathione (GSH), glutathione reductase (GR) and glutathione peroxidase (GPx) in TCON than NT but no differences in plasma lipid peroxidation (TBARS) and protein carbonylation (PC). However, total thiol (TT) concentration was two-fold lower in TCON than NT group. -Lipoic acid variously influenced the post-exercise levels of GSH (+40%), GR (-24%) and GPx (+29%), but markedly reduced by over 30% the resting and post-exercise TBARS and PC in TALA compared with TCON. TT concentration significantly increased in TALA but it did not reach the high level which was found in untrained group. It is concluded that -lipoic acid supplementation diminishes oxidative damage. It does not abolish differences in glutathione antioxidant system between untrained and trained subjects but modulates a pro-antioxidant response to the muscle-damaging exercise.

9

Oxidative stress and antioxidant responses in olive tree subjected to cover crops under rainfed conditions

63%

Correia C. , Brito C. , Santos D. , Bacelar E. , Goncalves B. , Ferreira H. , Moutinho-Pereira J. , Rodrigues M.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

|

nr 2

10

Protective effects of melatonin against oxidative damage of macromolecules caused by selected potential carcinogens

63%

Karbownik-Lewińska M. , Lewiński A.

Folia Medica Lodziensia

|

2010

|

tom 37

|

nr 1

57-67

EN

Reactive oxygen species (ROS) and free radicals are essential for physiological processes in living organisms. However, an overproduction of ROS and free radicals results in enhanced oxidative stress and can lead to several diseases, cancer included. Certain carcinogens may produce ROS, which directly damage macromolecules, leading to cancer initiation. It is expected that melatonin, as a well documented antioxidant, may protect macromolecules against oxidative damage caused by certain carcinogens possessing prooxidative properties. Experimental evidence for the subject in question has been discussed in the survey.

PL

Reaktywne formy tlenu (ROS) i wolne rodniki odgrywają istotną rolę w przebiegu procesów fizjologicznych w organizmach Ŝywych. Nadmierne wytwarzanie ROS i wolnych rodników moŜe jednakŜe prowadzić do nasilenia stresu oksydacyjnego i – w efekcie – do wyindukowania wielu chorób, w tym nowotworów złośliwych. Niektóre kancerogeny mogą indukować wytwarzanie ROS, które – następnie – uszkadzają makrocząsteczki w sposób bezpośredni, wiodąc do inicjacji nowotworzenia. UwaŜa się, Ŝe melatonina, jako dobrze udokumentowana substancja antyoksydacyjna, moŜe zapobiegać uszkodzeniom oksydacyjnym makrocząsteczek wywołanym przez niektóre kancerogeny posiadające właściwości prooksydacyjne; w pracy przedstawiono dowody doświadczalne dotyczące powyŜszych efektów melatoniny.

11

Does senescence correlate with oxidative damage in tobacco leaves?

63%

Pilarska M. , Krupinska K. , Niewiadomska E.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2013

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tom 94

|

nr 2

12

The involvement of oxidative stress in determining the severity and progress of pathological processes in dystrophin-deficient muscles

63%

Niebroj-Dobosz I. , Hausmanowa-Petrusewicz I.

Acta Biochimica Polonica

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2005

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tom 52

|

nr 2

EN

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.

13

Radiation induced oxidative DNA base damage and its repair in liver chromatin DNA of rats upon whole body gamma-irradiation

63%

Zastawny T. H. , Czerwinska B. , Drzewiecka B. , Olinski R.

Acta Biochimica Polonica

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1996

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tom 43

|

nr 3

EN

The amount of all bases, except for 5,6-dihydroxyuracil were significantly increased in rat DNA upon cobalt-60 y-irradiation. Control values were recovered 12 h after irradiation. The extent of DNA damage and repair was different for particular bases.

14

The effect of oxidative damage on ATP level in heat stressed endothelial cells

63%

Gray C. C. , Smolenski R. T. , Amrani M. , Taylor G. , Yacoub M. H.

Cellular and Molecular Biology Letters

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1999

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tom 04

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nr 3

15

Miscoding properties of isoguanine [2-oxoadenine] studied in an AMV reverse transcriptase in vitro system

63%

Bukowska A. M. , Kusmierek J. T.

Acta Biochimica Polonica

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1996

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tom 43

|

nr 1

EN

We have found that isoguanine (¡G) can pair with thymine (iG T) and the non- natural base, 5-methylisocytosine (iG x iCM) during template directed synthesis catalyzed by AMV reverse transcriptase. The ratio of these pairings is about 1:10, irrespectively which of the templates, poly(C,iG) or poly(I,iG) is used. This ratio corresponds to the ratio of 2-OH and 2-keto tautomers in monomer in aqueous sol ution and apparently it is not influenced by the template context. Our results indicate also that formation of the reverse transcriptase catalyzed base pairs between iG and A, G or C can occur only at a low frequency, comparable to the frequency, of mismatches of.

16

Intratracheally administrated corticosteroids improve lung function in meconium instilled rabbits

51%

Mokra D. , Mokry J. , Drgova A. , Petraskova M. , Bulikova J. , Calkovska A.

Journal of Physiology and Pharmacology. Supplement

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2007

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tom 58

|

nr 5

17

Differences in oxidative status, lung function, and pulmonary surfactant during long-term inhalation of medical oxygen and partially ionized oxygen in guinea pigs

51%

Calkovska A. , Engler I. , Mokra D. , Drgova A. , Sivonova M. , Tatarkova Z. , Calkovsky V. , Brozmanova M. , Tatar M.

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nr 6

173-181

18

Association between body iron stores and level of oxidatively modified DNA bases

51%

Dziaman T. , Jurgowiak M. , Olinski R.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

|

2011

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tom 92

|

nr 2

19

Hybrid cells differentiate to hepatic lineage cells and repair oxidative damage

51%

Xu D. , Wang F. , Gu H. , Wang J. , Guo Q. , Zhang Y. , Wang Z.

Cellular and Molecular Biology Letters

|

2010

|

tom 15

|

nr 3

451-472

EN

Hybrid cells derived from stem cells play an important role in organogenesis, tissue regeneration and cancer formation. However, the fate of hybrid cells and their range of function are poorly understood. Fusing stem cells and somatic cells induces somatic cell reprogramming, and the resulting hybrid cells are embryonic stem cell-like cells. Therefore, we hypothesize that fusion-induced hybrid cells may behave like ES cells in certain microenvironments. In this study, human hepatic cells were induced to apoptosis with H2O2, and then co-cultured with hybrid cells that had been derived from mouse ES cells and human hepatic cells using a transwell. After co-culturing, the degree of apoptosis was evaluated using Annexin-V/PI double-staining analysis, flow cytometry and Western-blot. We observed that H2O2-induced cell apoptosis was inhibited by co-culture. In addition, the activity of injury-related enzymes (GSH-Px, LDH and SOD) and the level of albumin release in the co-culture system trended toward the level of normal undamaged hepatic cells. The stably increased levels of secretion of ALB in the co-culture system also confirmed that co-culture with hybrid cells helped in recovery from injury. The fate of the hybrid cells was studied by analyzing their gene expression and protein expression profiles. The results of RT-PCR indicated that during co-culturing, like ES cells, hybrid cells differentiated into hepatic lineage cells. Hybrid cells transcripted genes from both parental cell genomes. Via immunocytochemical analysis, hepatic directional differentiation of the hybrid cells was also confirmed. After injecting the hybrid cells into the mouse liver, the GFP-labeled transplanted cells were distributed in the hepatic lobules and engrafted into the liver structure. This research expands the knowledge of fusion-related events and the possible function of hybrid cells. Moreover, it could indicate a new route of differentiation from pluripotent cells to tissue-specific cells via conditional co-culture.

20

Anti-glycemic and anti-hepatotoxic effects of mangosteen vinegar rind from Garcinia mangostana against HFD/STZ-induced type II diabetes in mice

51%

Karim N. , Jeenduang N. , Tangpong J.

Polish Journal of Food and Nutrition Sciences

|

2018

|

tom 68

|

nr 2

EN

This study focuses on anti-glycemic and anti-hepatotoxic effects of mangosteen vinegar rind (MVR) on fi ve weeks high-fat diet (HFD) / single dose streptozotocin (STZ) 30 mg/kg BW induced male ICR diabetic mice. Mice were randomly divided into fi ve groups (n=6), normal control, diabetic control, and diabetic groups treated with MVR 100, 200 mg/kg BW and glibenclamide 60 mg/kg BW for one week. After the treatment, lipid profi le, glycogen and bilirubin contents, oxidative damage (malondialdehyde, MDA), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) were measured in plasma and/or liver tissues. MVR and glibenclamide treatment to HFD/STZ-induced diabetic mice signifi cantly reduced their plasma glucose, plasma lipid profi le, and hepatic lipid profi le (P<0.05). Increased hepatic glycogen content indicates improvement of insulin sensitivity. Moreover, oxidative damage markers were ameliorated in MVR- and glibenclamide-treated groups compared to the diabetic control group. MVR with phenolic compounds content of 75 mg GAE/g dry weight and antioxidant potential of 303 mmol/L Trolox/g dry weight acted as a hepatoprotective agent against oxidative damage.