Matrix metalloproteinases (MMPs) are involved in tumour invasion and metastasis of colorectal carcinoma. Oxidative stress represents one of the possible mechanisms that activate inactive MMPs. Oxidative stress increases lipid peroxidation, which causes impaired membrane permeability and leakage of lactate dehydrogenase (LDH) and malate dehydrogenase (MDH) into circulation. Our aim was to assess the activity of MMP-2 and MMP-9 and its relation to the parameters of oxidative stress and membrane damage markers in patients with different TNM (tumour, lymph nodes, metastasis) stages of colorectal carcinoma. MMP-2 and -9 activities were evaluated by gelatin zymography. Oxidative stress was examined by quantifying serum malondialdehyde (MDA) concentration. LDH and MDH activities were determined spectrophotometrically. The activities of MMP-2 and -9 were significantly higher in the sera of colorectal carcinoma patients when compared to healthy subjects. There was a stage-dependent increase in relative MMP-2 activity compared to the overall serum gelatinolytic activity. The activity of MMP-9 was the highest in TNM III. The MDA concentration and the LDH and MDH activities were significantly higher in colorectal carcinoma patients than in controls, while LDH and MDH activities were stage dependent. There was significant correlation between serum MMP-2 and LDH activity in TNM II, III and IV patients. A stage-dependent increase of LDH and MDH activity was observed. We highlight here that MMP-9 could be a 100% sensitive marker of TNM stage III of colorectal carcinogenesis. In this study it was shown for the first time that gelatinolytic activity in colorectal carcinoma is associated with redox imbalance.

• MeSH
• kolorektální nádory metabolismus   MeSH
• lidé MeSH
• lipidové peroxidy metabolismus   MeSH
• malátdehydrogenasa metabolismus   MeSH
• matrixová metaloproteinasa 2 metabolismus   MeSH
• matrixová metaloproteinasa 9 metabolismus   MeSH
• peroxidy metabolismus   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH

Singlet oxygen (1O2) is formed by triplet-triplet energy transfer from triplet chlorophyll to O2 via Type II photosensitization reaction in photosystem II (PSII). Formation of triplet chlorophyll is associated with the change in spin state of the excited electron and recombination of triplet radical pair in the PSII antenna complex and reaction center, respectively. Here, we have provided evidence for the formation of 1O2 by decomposition of protein hydroperoxide in PSII membranes deprived of Mn4O5Ca complex. Protein hydroperoxide is formed by protein oxidation initiated by highly oxidizing chlorophyll cation radical and hydroxyl radical formed by Type I photosensitization reaction. Under highly oxidizing conditions, protein hydroperoxide is oxidized to protein peroxyl radical which either cyclizes to dioxetane or recombines with another protein peroxyl radical to tetroxide. These highly unstable intermediates decompose to triplet carbonyls which transfer energy to O2 forming 1O2. Data presented in this study show for the first time that 1O2 is formed by decomposition of protein hydroperoxide in PSII membranes deprived of Mn4O5Ca complex.

• MeSH
• chlorofyl metabolismus   MeSH
• elektronová paramagnetická rezonance metody   MeSH
• fotosystém II - proteinový komplex metabolismus   MeSH
• kyslík metabolismus   MeSH
• oxidace-redukce MeSH
• peroxid vodíku metabolismus   MeSH
• peroxidy metabolismus   MeSH
• přenos energie fyziologie   MeSH
• singletový kyslík metabolismus   MeSH
• světlo MeSH
• světlosběrné proteinové komplexy metabolismus   MeSH
• Publikační typ
• časopisecké články MeSH

Despite a high toxicity, paraquat is one of the most widely used herbicides in the world. Our study evaluated the effect of paraquat exposure on antioxidant response and locomotion activity in Drosophila melanogaster. We examined the enzymatic activity of superoxide dismutase (SOD) and catalase, and the transcript levels of both enzymes. Flies were exposed to a wide range of paraquat concentrations (0.25 μM to 25 mM) for 12 h. SOD, at both transcript and enzymatic levels, revealed a biphasic dose-response curve with the peak at 2.5 μM paraquat. A similar dose-response curve was observed at transcript levels of catalase. Males revealed higher susceptibility to paraquat exposure, displaying higher lethality, increased levels of SOD activity, and increased peroxide levels than in females. We found that the exposure of females to 2.5 μM paraquat leads to an increase in locomotion activity. Because susceptibility to paraquat was enhanced by mating, the study supports the hypothesis of elevation of stress sensitivity as a physiological cost of reproduction.

• MeSH
• antioxidancia metabolismus   MeSH
• chování zvířat účinky léků   MeSH
• Drosophila melanogaster účinky léků   metabolismus   MeSH
• herbicidy toxicita   MeSH
• katalasa metabolismus   MeSH
• oxidace-redukce MeSH
• paraquat toxicita   MeSH
• peroxidy metabolismus   MeSH
• rozmnožování účinky léků   MeSH
• sexuální faktory MeSH
• superoxiddismutasa metabolismus   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

It has been demonstrated that pterostilbene inhibits reactive oxygen species production in neutrophils in vitro. However, little is known about its effects on neutrophils during inflammation in vivo. In this study, the effect of pterostilbene on neutrophil activity was investigated in experimental arthritis model. Lewis rats were injected by a single intradermal injection of heat-killed Mycobacterium butyricum in Freund's adjuvant to develop arthritis. Another group of arthritic animals received pterostilbene 30 mg/kg, daily, p.o. The number and activity of neutrophils in blood were measured on a weekly basis during the whole experiment. Moreover, the total radical trapping potential in plasma was measured at the end of the experiment. In the pterostilbene treated arthritic group, the treatment significantly lowered the number of neutrophils in blood on days 14 and 21 without significant downregulation of neutrophil oxidative burst. Pterostilbene nonsignificantly increased total radical trapping potential in arthritic animals. These results indicate that the promising effects of pterostilbene on reactive oxygen species operate by different mechanisms in vitro and in the animal model of inflammation. In conclusion, the positive effects of pterostilbene in the model of arthritis may be attributed to regulation of neutrophil number.

• MeSH
• artritida experimentální farmakoterapie   patologie   MeSH
• down regulace účinky léků   MeSH
• krysa rodu rattus MeSH
• modely nemocí na zvířatech MeSH
• nepřímá aktivace účinky léků   imunologie   MeSH
• neutrofily cytologie   účinky léků   patologie   MeSH
• peroxidy metabolismus   MeSH
• počet leukocytů MeSH
• potkani inbrední LEW MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• stilbeny chemie   farmakologie   terapeutické užití   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

We describe a new method for the analysis of mitochondrial swelling curves. Using classical swelling curves, only the maximum extent of the swelling can be calculated in a numerical form. However, taking the derivative of the classical swelling curves enables the evaluation of two additional parameters of the swelling process in a numerical form, namely, the maximum swelling rate after the addition of the swelling inducer (as dA520/10 s) and the time (in sec) at which the maximum swelling rate after the addition of the swelling inducer is obtained. The use of these three parameters enables the better characterization of the swelling process as demonstrated by the evaluation of calcium and phosphate interactions in the opening of the mitochondrial permeability transition pore and by the characterization of the peroxide potentiating action.

• MeSH
• fosfáty metabolismus   MeSH
• intracelulární membrány metabolismus   MeSH
• jaterní mitochondrie metabolismus   MeSH
• krysa rodu rattus MeSH
• permeabilita MeSH
• peroxidy metabolismus   MeSH
• potkani Wistar MeSH
• transportní proteiny mitochondriální membrány metabolismus   MeSH
• vápník metabolismus   MeSH
• zduření mitochondrií fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

The abc1(-)/coq8(-) gene deletion respiratory-deficient mutant NBp17 of fission yeast Schizosaccharomyces pombe displayed a phenotypic fermentation pattern with enhanced production of glycerol and acetate, and also possessed oxidative stress-sensitive phenotypes to H(2)O(2), menadione, tBuOOH, Cd(2+), and chromate in comparison with its parental respiratory-competent strain HNT. As a consequence of internal stress-inducing mutation, adaptation processes to restore the redox homeostasis of mutant NBp17 cells were detected in minimal glucose medium. Mutant NBp17 produced significantly increased amounts of O(2)•- and H(2)O(2) as a result of the decreased internal glutathione concentration and the only slightly increased glutathione reductase activity. The Cr(VI) reduction capacity and hence the •OH production ability were decreased. The mutant cells demonstrated increased specific activities of superoxide dismutases and glutathione reductase (but not catalase) to detoxify at least partially the overproduction of reactive oxygen species. All these features may be explained by the decreased redox capacity of the mutant cells. Most notably, mutant NBp17 hyperaccumulated yellow CdS.

• MeSH
• ABC transportéry genetika   MeSH
• delece genu MeSH
• fenotyp MeSH
• glutathion metabolismus   MeSH
• kadmium metabolismus   MeSH
• mikrobiální testy citlivosti MeSH
• oxidace-redukce MeSH
• oxidancia farmakologie   MeSH
• peroxidy metabolismus   MeSH
• Schizosaccharomyces pombe - proteiny genetika   MeSH
• Schizosaccharomyces účinky léků   genetika   metabolismus   MeSH
• ubichinon genetika   MeSH
• Publikační typ
• časopisecké články MeSH

OBJECTIVES: Chronic pancreatitis (CP) is a heterogeneous disease defined as chronic inflammatory changes of the pancreatic tissue caused by variety of aetiologies. Oxidative stress accompanying the inflammatory processes has been suggested as an important factor contributing to CP development. The aim of this study was to determine levels of lipid peroxidation products malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), together with nitrites and the total antioxidant capacity in the plasma of patients with CP and control subjects. DESIGN: One hundred and five patients with chronic pancreatitis and twenty seven healthy controls were included into this study. Levels of MDA and 4-HNE were analyzed using high-performance liquid chromatography. The total antioxidant capacity of plasma against peroxyl radicals was evaluated using chemiluminescent determination. Nitrites were determined using Griess reaction. Biochemical and haematological parameters were measured by standard methods. RESULTS: The plasma levels of both MDA and 4-HNE, together with the plasma levels of nitrites, were significantly higher in CP patients, compared to healthy controls. The total antioxidant capacity did not differ significantly. Biochemical parameters were in the normal range. The MDA and 4-HNE levels correlated positively with the levels of high-density lipoprotein cholesterol. Nitrite levels correlated positively with C-reactive protein, total white blood cells, and triglycerides. CONCLUSION: The significantly increased plasma levels of MDA, 4-HNE, and nitrites indicate that oxidative stress is present in patients with CP and that it may play a role in initiation and maintenance of inflammation within the pancreatic tissue in CP patients.

• MeSH
• aldehydy krev   MeSH
• antioxidancia metabolismus   MeSH
• C-reaktivní protein metabolismus   MeSH
• chronická pankreatitida krev   metabolismus   MeSH
• dospělí MeSH
• dusitany krev   MeSH
• HDL-cholesterol krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• luminiscenční měření MeSH
• malondialdehyd krev   MeSH
• oxidační stres MeSH
• peroxidy metabolismus   MeSH
• triglyceridy krev   MeSH
• vysokoúčinná kapalinová chromatografie MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

OBJECTIVES: The generation of reactive oxygen species (ROS) by phagocytes is one of the irreplaceable microbicidal tools of innate immunity. It has been reported in our previous studies that short-term treatment by carvedilol ex vivo inhibits ROS generation. The purpose of this study was to investigate the long-term effect of carvedilol on phagocytes. METHODS: Human leukemia HL-60 cells differentiated into granulocyte-like cells were used as the model. Final concentrations of carvedilol were 0.1-100 micromol/l. The production of ROS by HL-60 cells was measured using luminol-enhanced chemiluminescence (CL). RESULTS: Carvedilol in concentrations 0.1-10 micromol/l did not exhibit any toxic effect on cells (measured using bioluminescent bacteria Photorhabdus luminescens subsp. thracensis). One hour's treatment with 10 micromol/l carvedilol significantly decreased both spontaneous and activated CL of cells. Conversely, no inhibitory effects on CL were observed in 10 micromol/l carvedilol after 48 h incubation; lower concentrations of carvedilol even slightly increased the CL activity of HL-60 cells. A significant increase in spontaneous CL activity was detected in cells incubated with 10 micromol/l carvedilol in comparison with the control. Powerful antioxidative properties of carvedilol against peroxyl radical (ORAC assay) were proved. No scavenging of nitric oxide (electrochemical method) was observed. CONCLUSIONS: Long-term influence of carvedilol can induce an increase in the generation of phagocyte-derived ROS and potentially also other inflammatory mediators. The increased ROS production is compensated for by antioxidative properties of carvedilol although the increased production of inflammatory mediators could affect the proper function of immune system.

• MeSH
• adenosintrifosfát metabolismus   MeSH
• beta blokátory farmakologie   toxicita   MeSH
• buněčná diferenciace účinky léků   MeSH
• fagocyty účinky léků   MeSH
• fluorometrie MeSH
• granulocyty účinky léků   MeSH
• HL-60 buňky MeSH
• karbazoly farmakologie   toxicita   MeSH
• lidé MeSH
• luminiscence MeSH
• oxid dusnatý metabolismus   MeSH
• peroxidy metabolismus   MeSH
• proliferace buněk účinky léků   MeSH
• propanolaminy farmakologie   toxicita   MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH

OBJECTIVES: An increased glucose utilization by aldose reductase (ALR-2) has been implicated in the pathogenesis of diabetic vascular complications. In this process, several mechanisms are involved, including the depletion of cofactors required for the action of antioxidant enzymes or endothelial NO synthase. In this study, the effect of a novel ALR-2 inhibitor JMC-2004 on hyperglycemia-induced endothelial dysfunction was studied. METHODS: Bovine aortic endothelial cells (BAEC) were treated with glucose (30 mM), JMC-2004 (0.01mM), or glucose and JMC-2004 for 24 h. The cells were then stimulated with calcium ionophore A23187 after which NO production was measured electrochemically using a porphyrine-coated carbon NO electrode. Nitrite concentrations were determined in the cell supernatants. The peroxyl and hydroxyl radical-scavenging activity of JMC-2004 was measured with luminol-enhanced chemiluminescence. The expression of eNOS was determined by Western blotting. JMC-2004 IC50 for ALR-2 was determined colorimetrically with D-glyceraldehyde as a substrate. RESULTS: Incubating the cells with 30 mM glucose strongly diminished A23187- induced NO production. Treatment with JMC-2004 restored NO production by 40% without affecting eNOS expression. This effect was probably antioxidantindependent, since JMC-2004 did not have any antioxidant capacity. JMC-2004 exerted high selectivity towards ALR-2. CONCLUSIONS: ALR-2 inhibition with JMC-2004 was able to abolish hyperglycemia- induced endothelial dysfunction in bovine aortic endothelial cells.

• MeSH
• aldehydreduktasa antagonisté a inhibitory   MeSH
• buněčné linie MeSH
• calcimycin farmakologie   MeSH
• cévní endotel patologie   účinky léků   MeSH
• elektrochemie MeSH
• endoteliální buňky patologie   účinky léků   MeSH
• fenoly farmakologie   MeSH
• glukosa farmakologie   MeSH
• glyceraldehyd metabolismus   MeSH
• hydroxylový radikál metabolismus   MeSH
• hyperglykemie patologie   MeSH
• inhibitory enzymů farmakologie   MeSH
• luminiscence MeSH
• oxid dusnatý metabolismus   MeSH
• peroxidy metabolismus   MeSH
• pyrroly farmakologie   MeSH
• skot MeSH
• synthasa oxidu dusnatého, typ III metabolismus   MeSH
• western blotting MeSH
• zvířata MeSH
• Check Tag
• skot MeSH
• zvířata MeSH
• Publikační typ
• práce podpořená grantem MeSH

The aim of this study was to evaluate the contribution of three plasma antioxidants (albumin, uric acid, SH groups) to the plasma total peroxyl radical-trapping antioxidant capacity (TRAP) in 2 and 4 h of intestinal reperfusion in rats. TRAP increased significantly both after 2 and 4 h of reperfusion. Neither albumin nor SH groups contributed significantly to this increase. TRAP was strongly influenced by the increase in uric acid concentration and also probably by the cell destruction caused by oxidative stress. Since the TRAP increase was accompanied by an increase in the level of thiobarbituric acid reactive substances (TBARS, a marker of lipid peroxidation), we can conclude that even such a large increase in TRAP is not sufficient to prevent the progression of lipid peroxidation and oxidative stress.

• MeSH
• antioxidancia analýza   MeSH
• financování organizované MeSH
• ischemie MeSH
• krysa rodu rattus MeSH
• kyselina močová krev   MeSH
• oxidační stres MeSH
• peroxidace lipidů MeSH
• peroxidy metabolismus   MeSH
• potkani Wistar MeSH
• reaktivní formy kyslíku metabolismus   MeSH
• reperfuzní poškození patofyziologie   veterinární   MeSH
• sérový albumin MeSH
• sulfhydrylové sloučeniny krev   MeSH
• tenké střevo krevní zásobení   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH