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1

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

100%
Dziaman T., Jurgowiak M., Olinski R.
Biotechnologia
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2011
|
issue 2
159-165
EN
It appears that the presence of labile iron pool (LIP, iron not bound to proteins) in cells can result in the production of reactive oxygen species namely COH radical which may be responsible for the formation of 8-oxo-7,8-dihydro- 2N-deoxyguanosine (8-oxodG) in the cellular DNA. This oxidatively modified molecule is regarded as a good biomarker of cancer risk and a general index of oxidative stress in relation to other diseases. There are numerous data suggesting that oxidative stress may be involved in the development of cardiovascular diseases and cancer. It has been observed that heterozygosity for hereditary hemochromatosis (a disease with abnormal iron storage) is a risk factor for vascular diseases. Previously we have demonstrated higher levels of LIP in a group of atherosclerotic patients when compared with the control group. This suggests that LIP may increase the risk of disease development. The aforementioned condition may lead to oxidative stress, which is manifested by a higher level of 8-oxodG in blood lymphocytes, and may be one of the factors responsible for the development of cardiovascular diseases. We have also reported the relationship between LIP and the endogenous level of 8-oxodG in human lymphocytes of the colon cancer patients. Good correlation has been determined between LIP and oxidatively modified nucleoside. The results of our studies on piglets supplemented with iron dextran (FeDex) also show an increase in the 8-oxodG level in hepatic DNA. These findings confirm the possibility that iron overload may favor the persistence of harmful LIP which may catalyze generation of the potentially carcinogenic 8-oxodG moiety in the cellular DNA.
2

Adaptative mechanisms of the cell against oxidative stress and damage removal

100%
Farbiszewski R., Skrzydlewska E.
Postępy Higieny i Medycyny Doświadczalnej
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1996
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vol. 50
|
issue 6
613-620
EN
This review describe the role of adaptative mechanisms of the cell against oxidative damage induced by free radicals. Adaptative response refers the ability of cells to better resist the damaging effects of toxic agent when first preexposed to a lover dose. Extensive studies have revealed that oxidized proteins are recognized by proteases and completely degraded to amino acids. In this way damaged proteins are removed.
3

Lactoferrin and immunologic dissonance: clinical implications

80%
Kruzel M. L., Zimecki M.
Archivum Immunologiae et Therapiae Experimentalis
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2002
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vol. 50
|
issue 6
397-408
EN
Homeostasis is the maintenance of equilibrium in a biological system by means of positive and negative feedback control mechanisms that counteract influences tending toward physiological dissonance. At the molecular level, homeostasis is controlled by the network of the neuro-endocrine-immune system, in which lactoferrin plays a central role. The purpose of this review is to provide a comprehensive summary of a collaborative study established between the Hirszfeld Institute of Immunology and Experimental Therapy (Wroclaw, Poland) and the University of Texas Health Science Center (Huston, USA) regarding lactoferrin and its role in homeostasis. In our studies we focused on the immunoregulatory functions of lactoferrin, both in vitro and in vivo. We investigated the immune status of individuals subjected to different insults, including experimental endotoxemia in mice and surgery in humans. We also studied a lactoferrin-dependent delayed type hypersensitivity (DTH) response to evaluate some of the mechanisms by which lactoferrin can effectively substitute an adjuvant in vaccine.
4
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Role of serotonin in cerebral oxidative stress in rats

80%
Munoz-Castaneda J. R., Montilla P., Padillo F. J., Bujalance I., Munoz M. C., Muntane J., Tunez I.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
|
issue 1
1-6
EN
Serotonin or 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter synthesized by the aromatic amino acid decarboxylase using 5-hydroxytryptophan (5-HTP) as a substrate. It was recently shown that serotonin and its precursor have powerful antioxidant properties. The aim of this study was to evaluate the effect of reduction in 5-HT levels by para-chlorophenylalanine (pCPA) and their restoration by 5-HTP administration on lipid peroxidation and antioxidant status in rat brain. Serotonin levels were decreased by p-chlorophenylalanine administration. The effect of p-chlorophenylalanine was counteracted by the intraperitoneal administration of 5-hydroxytryptophan. We evaluated the concentration of serotonin, malonyl dialdehyde and the status of antioxidants (GSH, catalase and superoxide dismutase) in brain. The results showed that p-chlorophenylalanine (300 mg/kg) induced a depletion of serotonin concentration and antioxidant status, as well as enhancing malonyl dialdehyde concentration in brain. The exogenous administration of 5-hydroxytryptophan prevented all effects induced by p-chlorophenylalanine in brain tissue. The recovery of the neurotransmitter concentration in brain was related to the reduction of lipid peroxide generation and improved antioxidant status. In conclusion, our study supports the view that the antioxidant properties of serotonin protect against basal oxidative stress in brain.
5

Role of iron in pathogenesis of Parkinson disease

80%
Galazka-Friedman J., Friedman A.
Biotechnologia
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2011
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issue 2
153-158
EN
Parkinson's disease is one of the most frequent human neurodegenerations. Motor symptoms of Parkinson's disease are the consequence of the destruction of nervous cells in the substantia nigra (SN), a small (about 500 mg) structure located deep in human brain. The concentration of iron in SN is comparable to that in liver and is equal to about 180 ? 60 ng/mg of wet tissue and the iron in SN is mostly bound to ferritin. For many years it has been believed that the degeneration of nervous cells in SN in Parkinson's disease is related to an important increase in the concentration of iron. Our own studies based on M?ssbauer spectroscopy and other studies conducted with the use of various techniques have not confirmed this finding. The ratio of the concentration of iron in PD vs. control SN evaluated by Mossbauer spectroscopy was found to be equal 1.00?0.13. We also confirmed that most of iron in SN is located within ferritin. ELISA studies demonstrated a significant decrease in L ferritin in parkinsonian SN compared to the control group. As L-ferritin is related to safe keeping of iron within the ferritin shell, its decrease may lead to an efflux of iron and increase in the concentration of labile iron. Indeed our studies did show a difference in the concentration of labile iron between PD and control SN (135 +- 10 ng/g vs. 76 +- 5 ng/g). This labile iron, which may initiate Fenton reaction, may be the cause of the oxidative stress leading to the death of nervous cells in PD.
6
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Dynamics of expression of the mRNA for cytokines and inducible nitric synthase in a murine model of the Parkinson disease

80%
Ciesielska A., Joniec I., Przybylkowski A., Gromadzka G., Czlonkowska A., Czlonkowski A.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 2
117-126
EN
The inflammatory reaction and oxidative stress has been linked with PD. Proinflammatory cytokines promote neurodegeneration or neuroprotection in different animal models. In addition, these cytokines have been reported to increase iNOS expression. With the RT-PCR method we evaluated mRNA levels for IL1beta, IL6, TNF, IFN gamma, IL-10 and iNOS in the striatum of C57BL/6 mice after MPTP intoxication. The IL1beta mRNA expression rapidly increased, nad peaked at 6 h. The first increase of mRNA for TNFalpha and INFgamma was noticed at 6-24 h and the second at the 7th day after MPTP intoxication. Two peaks of IL10 mRNA were seen, immediately (6 h) and at the 3rd day post MPTP injection. The peak of mRNA level for IL6 was observed at the 7th day. Expression of mRNA for iNOS peaked at 24 h, started decreasing on the 3rd day, but was still present till the 14th day Those findings suggest that cytokine network and iNOS may be involved in the development of immune changes accompanying degeneration of the nigrostriatal system.
7

Glutathione in therapy

80%
Winiarska K., Drozak J.
Postępy Higieny i Medycyny Doświadczalnej
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2002
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vol. 56
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issue 4
521-536
EN
It has been commonly accepted that oxidative stress is involved in pathogenesis of many serious and even lethal health disturbances, including neurodegenerative diseases, diabetes, alcoholic disease, viral and bacterial infections. In this paper we discuss the protective antioxidative role of glutathione, the predominant non-protein thiol in mammalian cells. We also emphasize the perspectives of glutathione therapy i.e. application of both cysteine and glutathione precursors.
8

Do changes in iron metabolism contribute to the acceleration of the atherosclerosis process?

80%
Formanowicz D.
Biotechnologia
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2011
|
issue 2
180-192
EN
There are several risk factors whose association with atherosclerosis, a chronic disease with complicated etiology, is well established, including age, gender, smoking, lipids metabolism disorders, diabetes mellitus, obesity and reduced physical activity. Surprisingly, many cardiovascular related deaths occur in individuals without standard risk factors, so it has been suggested that these cases must be the result of other factors, previously not taken into account. This phenomenon resulted in the development of research focused on finding new risk factors. In 1981, Sullivan first postulated the so-called 'iron hypothesis', suggesting that the regular menstrual iron loss, rather than other known effects of estrogen, protects women against coronary heart disease. It is widely believed at present, that iron is an essential catalyst in the oxidation and oxidative modification of low-density lipoprotein cholesterol which appears to be one of the pivotal steps in the early phase of the formation of the atherosclerotic plaque. Thus, iron depletion through menstrual loss might reduce oxidative stress and beneficially affect atherogenesis. Stored iron appears to be essential in the process of atherogenesis which is strictly required for normal cellular metabolism but also serves as a reservoir from which toxic-active iron can be liberated under atherogenic stimuli and result in lipid peroxidation. In this process, two pathways i.e., iron homeostasis metabolic pathway and metabolic pathways involving proinflammatory cytokines are closely interconnected. In human monocytes, these cytokines also increase the uptake of non-transferrin-bound iron, via the stimulation of divalent metal transporter- 1 synthesis and cause iron retention by down-regulating ferroportin synthesis. It has been found recently that iron depositions are prominent in human atherosclerosis lesions. It can therefore be concluded that the results of scientific research, particularly those of the last ten years, provide a strong pathological basis to support the role of iron metabolism alterations in vascular damage and in the progression of atherosclerosis process.
9

Total antioxidant status and 8-hydroxydeoxyguanosine levels in gingival and peripheral blood of periodontitis patient

80%
Konopka T., Krol K., Kopec W., Gerber H.
|
|
issue 6
417-422
EN
Introduction: The aim of this study was to determine 8-OHdG concentration as a biomarker of oxidant-induced DNA damage and to assess total antioxidant status (TAS) in gingival and peripheral blood during periodontal lesion. Materials and Methods: The study included 56 untreated periodontitis patients (26 with aggressive periodontitis, and 30 with chronic periodontitis (CP). The control group consisted of 25 healthy volunteers without pathological changes in the periodontium. Competitive ELISA was used to measure 8-OHdG. A colorimetric method based on the reduction of ABTSo+ radical cation generation was used to measure TAS. Results: Significantly higher 8-OHdG concentrations were detected in the gingival blood in both groups of patients with periodontitis than in the control group. Subjects with CP had significantly decreased TAS levels in the gingival blood compared with the control group. A significantly decreased TAS level in the peripheral blood in both patient groups compared with the control group was found. Significant positive correlation between TAS levels in venous and gingival blood in all the periodontitis patients and in the CP group was observed. Conclusions: The oxidative burst in periodontitis may lead to significant local damage to nucleic acids. The significantly decreased TAS level in the gingival blood of CP patients compared with the healthy subjects suggests the possibility of a significant decrease in local antioxidant system capacity during the course of periodontitis. The decreased TAS level in the peripheral blood in the group of all patients with periodontitis may be one of the pathogenic mechanisms underlying the links between periodontal disease and several systemic diseases for which periodontitis is regarded as a independent risk factor.
10

Influence of alcohol dependence on oxidative stress parameters

80%
Kopczynska E., Torlinski L., Ziolkowski M.
|
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vol. 55
|
issue 1
95-111
EN
The toxic of ethanol on pro-oxidant balance has been discussed. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. Role of acetaldehyde in ethanol-induced oxidative stress has been stressed.
11
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Melatonin attenuates radiation-induced learning deficit and brain oxidative stress in mice

70%
Manda K., Anzai K., Kumari S., Bhatia A. L.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 1
63-70
EN
Oxidative stress has been implicated in cognitive impairment in both experimental animals and humans. This implication has led to the notion that antioxidant defence mechanisms in the brain are not sufficient to prevent oxidative damage, and that dietary intake of a variety of antioxidants might be beneficial for preserving brain function. The present study, therefore, aimed to investigate the protective effect of melatonin against radiation-induced impairment in the learning ability of mice. Twenty days oral administration of melatonin (0.1 mg/kg b.w.), followed by an acute exposure to gamma-radiation (6 Gy), inhibited the radiation-induced decline in learning ability. Biochemical estimation of brain protein carbonyls, malondialdehide (MDA) and reduced glutathione (GSH) in these mice indicated that radiation-induced augmentation of protein oxidation and lipid peroxidation had been significantly ameliorated in melatonin treated, irradiated mice. Radiation-induced deficit of glutathione was also normalized by melatonin administration, as there was no statistical difference from normal at P<0.001. Results indicate the antioxidative as well as neuroprotective properties of melatonin against the radiation. These findings support results showing melatonin as a free radical scavenger.
12

Genome-wide identification of genes involved in tolerance to various environmental stresses in Saccharomyces cerevisiae

70%
Auesukaree C., Damnernsawad A., Kruatrachue M., Pokethitiyook P., Boonchird C., Kaneko Y., Harashima S.
Journal of Applied Genetics
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2009
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vol. 50
|
issue 3
301-310
EN
During fermentation, yeast cells are exposed to a number of stresses ? such as high alcohol concentration, high osmotic pressure, and temperature fluctuation ? so some overlap of mechanisms involved in the response to these stresses has been suggested. To identify the genes required for tolerance to alcohol (ethanol, methanol, and 1-propanol), heat, osmotic stress, and oxidative stress, we performed genome-wide screening by using 4828 yeast deletion mutants. Our screens identified 95, 54, 125, 178, 42, and 30 deletion mutants sensitive to ethanol, methanol, 1-propanol, heat, NaCl, and H2O2, respectively. These deleted genes were then classified based on their cellular functions, and cross-sensitivities between stresses were determined. A large number of genes involved in vacuolar H+-ATPase (V-ATPase) function, cytoskeleton biogenesis, and cell wall integrity, were required for tolerance to alcohol, suggesting their protective role against alcohol stress. Our results revealed a partial overlap between genes required for alcohol tolerance and those required for thermotolerance. Genes involved in cell wall integrity and the actin cytoskeleton are required for both alcohol tolerance and thermotolerance, whereas the RNA polymerase II mediator complex seems to be specific to heat tolerance. However, no significant overlap of genes required for osmotic stress and oxidative stress with those required for other stresses was observed. Interestingly, although mitochondrial function is likely involved in tolerance to several stresses, it was found to be less important for thermotolerance. The genes identified in this study should be helpful for future research into the molecular mechanisms of stress response.
13

Lactic acid bacteria cellular responses for enviromental stress

70%
Sadowska J., Grajek W.
Biotechnologia
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2009
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issue 4
115-132
EN
Lactic acid bacteria (LAB) constitute a heterogeneous group of bacteria that are traditionally used to produce fermented foods. The industrialization of food biotransformations increased the economical importance of LAB. The development of new applications such probiotic foods reinforces the need for robust LAB. They have to survive in the digestive tract, and express specific functions under conditions that are unfavorable to growth. A better understanding of the mechanisms of stress resistance and LAB cellular responses should allow to prepared these bacteria for industrial processes. Range of examples of diferent enviromental stress, related genes and molecular mechanisms of the stress responses are presented.
14

Concentration of TBA-reactive substances in type II pneumocytes exposed to oxidative stress

70%
Piotrowski W. J., Marczak J., Kurmanowska Z., Gorski P.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
435-440
EN
Oxidative lung damage may be associated with the destruction of alveolar cells. Type II alveolar epithelial cells (AECs), as progenitors of type I cells, are indispensable for the renovation of alveolar structure after lung injury. Extensive damage to type II cells could be responsible for unfavorable outcome. However, the susceptibility of type II AECs to oxidative stress is unclear. Materials We investigated the susceptibility of freshly isolated and cultured rat type II AECs to and Methods: oxidative stress (H2O2 and Fe2+). Thiobarbituric acid reactive substances (TBARS) were measured as indices of lipid peroxidation and cytotoxicity was estimated by the MTT test. Aminotriazol (ATZ), an inhibitor of intracellular catalase, was used to estimate the protective role of catalase. Results: TBARS concentration increased significantly in freshly isolated, oxidant-exposed cells (4.0?1.3 vs. 8.3?2.2 nmol/g protein, p=0.0313) and insignificantly in cultured cells (1.7?0.4 vs. 4.4?1.7 nmol/g protein). ATZ was toxic even to cells not exposed to oxidants. Inhibition of catalase in cells exposed to oxidants resulted in an insignificant increase in TBARs: 4.5?1.5 vs. 16.2?3.9 nmol/g protein, p=0.0625, and 4.0?0.8 vs.7.6?4.0 for freshly isolated and cultured cells, respectively. Oxidative stress itself did not increase cytotoxicity. Conclusions: Type II AECs are not resistant to oxidative stress. We cannot, however, explain why cells with evidence of lipid peroxidation do not show increased cytotoxicity. The toxicity of ATZ is not related to oxidative cell damage. In cells exposed to oxidants, TBARS may further increase when catalase is inhibited, which suggests an important protective role for catalase.
15

Biological properties of lipoic acid

61%
Bilska A., Wlodek L.
Postępy Higieny i Medycyny Doświadczalnej
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2002
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vol. 56
|
issue 2
201-219
EN
Lipoic acid is a prostetic group of H-protein of the glycine cleavage system and the dihydrolipoamide acyltransferases (E2) of the pyruvate, alpha-ketoglutarate and branched-chain alpha-keto acid dehydrogenase complexes. Lipoic acid and its reduced form, dihydrolipoic acid, reacts with oxygen reactive species. This paper reviews the beneficial effects in oxidative stress models or clinical conditions.
16

The influence of environmental stresses on Saccharomyces cerevisiae yeast in ethanol fermentation

61%
Grajek W., Szymanowska D.
Biotechnologia
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2008
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issue 3
46-63
EN
The development of ethanol fermentation process brings numerous environmental stresses influenced by the survival and metabolism of industrial microorganisms. Saccharomyces cerevisiae strains have evolved to survive constant fluctuation in their external surroundings by special adaptation systems. These adaptation mechanisms involve reorganization of genomic expression by activation of transcriptional factors under stress conditions and production of suitable metabolites increased by cell survival. This review is focused on the metabolism and genetic response of cells to diverse environmental changes, especially to heat, osmotic, ethanol, oxidative, toxic and other physic-chemical stresses.
17
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Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

51%
Zekanowski C., Wojda U.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 2
232-253
EN
Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Chromosome missegregation was proposed two decades ago to be responsible for neurodegeneration in AD patients. It was speculated that the aneuploidy is a result of aberrant cell cycle of neuronal progenitors during adult neurogenesis and/or of mature neurons. There is mounting evidence of increased rate of general aneuploidy and cell cycle reentry in the AD patients' brains, with area-specific pattern. In this review, we discuss the involvement of chromosome instability, genome damage and cell cycle impairment in AD pathology.
18
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Alzheimer's beta-amyloid peptide as a source of neurotoxic free radicals: the role of structural effects

41%
Pogocki D.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 2
131-145
EN
This mini review gives a brief overview over the oxidation mechanism of methionine (Met), relevant for processes which may lead to the oxidation of amyloid beta-peptide (betaAP), involved in the pathogenesis of Alzheimer?s disease. The Cu II-catalysed oxidation of C-terminal Met 35 in AP depends on the secondary structure of the peptide. That seems to be the key to the known propensities of this peptide to form reactive oxygen species and free radicals. The pro-oxidant character of betaAP is not associated with its -beta sheet insoluble form. On the contrary, the alpha-helically organised structure is responsible for betaAP redox-related cytotoxicity.
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