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    Wyświetlanie 1-5 z 5
    Tytuł:
    Allelic polymorphism of endothelial NO-synthase gene and its functional manifestations
    Autorzy:
    Dosenko, Victor
    Zagoriy, Vyacheslav
    Haytovich, Nikolay
    Gordok, Olga
    Moibenko, Alexey
    Powiązania:
    https://bibliotekanauki.pl/articles/1041240.pdf
    Data publikacji:
    2006
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    activity of nitric oxide synthase
    endothelial nitric oxide synthase
    RNA expression
    platelets
    allelic polymorphism
    Opis:
    Investigation of the mechanisms of phenotypic realization of allelic polymorphism of the eNOS gene has shown that the level of eNOS mRNA and activity of this enzyme in platelets depends from genotype. We identified a T-786→C polymorphism in the promoter region, a variable number of tandem repeats (4a/4b) in intron 4 and the G894→T polymorphism in exon 7 of the eNOS gene in isolated human platelets. We measured eNOS mRNA in isolated platelets by reverse transcription-PCR and eNOS enzyme activity by fluorimetric detection system FCANOS-1 using diaminofluorescein diacetate (DAF-2A). It was shown that the level of eNOS mRNA is the lowest for the -786C/C promoter genotype. In exon 7 homozygotes (894T/T) the level of RNA is lower than in normal homozygotes (894G/G), but higher than in heterozygotes (894G/T). The eNOS activity in platelets is lower in carriers of the 786C/C promoter genotype than in normal homozygotes (2.1 × P=0.03), and lower comparing to heterozygotes (2.9 × P>0.05). The eNOS activity accompanying the 894T/T variant of exon 7 is also lower than in normal homozygotes (P>0.05). Regarding the polymorphism in intron 4 - the enzyme's activity is lower in carriers of the 4a/4a genotype comparing to normal homozygotes (1.7 × P>0.05) and lower than in heterozygotes (1.9 × P>0.05). These results allow one to conclude that the T-786→C polymorphism of the eNOS gene promoter most significantly affects the gene expression and eNOS activity.
    Źródło:
    Acta Biochimica Polonica; 2006, 53, 2; 299-302
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Polymorphism in intron 23 of the endothelial nitric oxide synthase gene (NOS3) is not associated with hypertension.
    Autorzy:
    Derebecka, Natalia
    Hołysz, Marcin
    Dankowski, Rafał
    Wierzchowski, Michał
    Trzeciak, Wiesław
    Powiązania:
    https://bibliotekanauki.pl/articles/1043838.pdf
    Data publikacji:
    2002
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    nitric oxide synthase
    gene polymorphism
    hypertension
    intron 23
    Opis:
    Nitric oxide (NO) is synthesised in the vascular endothelium by nitric oxide synthase (NOS3) and is an important factor in the regulation of blood pressure. Impaired synthesis of NO due to mutations in the NOS3 gene is associated with hypertension. To date several allelic variants of the NOS3 gene have been identified and their possible linkage with hypertension investigated. We studied the distribution of genotypes and frequency of alleles of the G11T polymorphism in intron 23 of the NOS3 gene in patients with hypertension and in a control group of healthy individuals. The polymorphism was determined by PCR-RFLP analysis. The distribution of genotypes in the patients with hypertension and in the healthy individuals did not differ significantly from the values predicted from Hardy-Weinberg equilibrium for the general population. No major differences in the distribution of the G11T polymorphism in the patients and healthy individuals were found (P > 0.05).
    Źródło:
    Acta Biochimica Polonica; 2002, 49, 1; 263-268
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Influence of elastin-derived peptides, glucose, LDL and oxLDL on nitric oxide synthase expression in human umbilical artery endothelial cells
    Autorzy:
    Garczorz, Wojciech
    Francuz, Tomasz
    Gmiński, Jan
    Likus, Wirginia
    Siemianowicz, Krzysztof
    Jurczak, Teresa
    Strzałka-Mrozik, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1039891.pdf
    Data publikacji:
    2011
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    nitric oxide synthase
    oxidized LDL
    LDL
    EDP
    atherosclerosis
    hyperglycemia
    endothelium
    elastin-derived peptides
    eNOS
    Opis:
    Endothelial dysfunction plays an important role in the development of atherosclerosis. Elastin-derived peptides (EDP), hyperglycemia, hypercholesterolemia and oxidized LDL have a proven proatherosclerotic potential. Nitric oxide generated by endothelial nitric oxide synthase (eNOS; EC 1.14.13.39) is an important vasorelaxant. Here we studied the influence of those proatherosclerotic factors on eNOS gene and protein expression in artery-derived endothelial cells. Human umbilical artery endothelial cells (HUAEC) were incubated with or without: glucose (270 mg/dl), LDL (200 mg/dl), oxidized LDL (oxLDL 25 mg/dl) or κ-elastin (0.5 and 2.5 µg/ml). Gene expression was assessed by real time RT-PCR, whilst the eNOS protein by ELISA. In cells incubated with 2.5 µg/ml of κ-elastin, a 31 % increase of eNOS mRNA expression was observed, but the protein level remained unchanged. OxLDL, LDL and glucose decreased the eNOS protein level by 74 %, 37 % and 29 %, respectively. OxLDL decreased eNOS mRNA by 42 %. LDL non-significantly decreased eNOS mRNA expression. An elevated glucose level did not affect the eNOS mRNA expression. Hyperglycemia and an elevated level of LDL, particularly oxLDL, decreased the level of eNOS protein in endothelial cells. As κ-elastin did not decrease the expression of eNOS gene in HUAEC, the proatherogenic properties of elastin-derived peptides are unlikely to be due to their influence on eNOS.
    Źródło:
    Acta Biochimica Polonica; 2011, 58, 3; 375-379
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Single-electron reduction of quinone and nitroaromatic xenobiotics by recombinant rat neuronal nitric oxide synthase
    Autorzy:
    Anusevičius, Žilvinas
    Nivinskas, Henrikas
    Šarlauskas, Jonas
    Sari, Marie-Agnes
    Boucher, Jean-Luc
    Čėnas, Narimantas
    Powiązania:
    https://bibliotekanauki.pl/articles/1039577.pdf
    Data publikacji:
    2013
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    antitumour agents
    nitroaromatic compounds
    electron transfer mechanism
    oxidative stress
    quinones
    Neuronal nitric oxide synthase (nNOS)
    Opis:
    We examined the kinetics of single-electron reduction of a large number of structurally diverse quinones and nitroaromatic compounds, including a number of antitumour and antiparasitic drugs, and nitroaromatic explosives by recombinant rat neuronal nitric oxide synthase (nNOS, EC 1.14.13.39), aiming to characterize the role of nNOS in the oxidative stress-type cytotoxicity of the above compounds. The steady-state second-order rate constants (kcat/Km) of reduction of the quinones and nitroaromatics varied from 102 M-1s-1 to 106 M-1s-1, and increased with an increase in their single-electron reduction potentials (E17). The presence of Ca2+/calmodulin enhanced the reactivity of nNOS. These reactions were consistent with an 'outer sphere' electron-transfer mechanism, considering the FMNH./FMNH2 couple of nNOS as the most reactive reduced enzyme form. An analysis of the reactions of nNOS within the 'outer sphere' electron-transfer mechanism gave the approximate values of the distance of electron transfer, 0.39-0.47 nm, which are consistent with the crystal structure of the reductase domain of nNOS. On the other hand, at low oxygen concentrations ([O2] = 40-50 μM), nNOS performs a net two-electron reduction of quinones and nitroaromatics. This implies that NOS may in part be responsible for the bioreductive alkylation by two-electron reduced forms of antitumour aziridinyl-substituted quinones under a modest hypoxia.
    Źródło:
    Acta Biochimica Polonica; 2013, 60, 2; 217-222
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Amyloid beta enhances cytosolic phospholipase A2 level and arachidonic acid release via nitric oxide in APP-transfected PC12 cells
    Autorzy:
    Chalimoniuk, Małgorzata
    Stolecka, Anna
    Cąkała, Magdalena
    Hauptmann, Susane
    Schulz, Kris
    Lipka, Uta
    Leuner, Kristine
    Eckert, Anne
    Muller, Walter
    Strosznajder, Joanna
    Powiązania:
    https://bibliotekanauki.pl/articles/1041051.pdf
    Data publikacji:
    2007
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    nitric oxide synthase
    amyloid beta
    calcium
    arachidonic acid
    antioxidative enzymes
    reactive oxygen species
    cytosolic phospholipase A_2
    mitochondria
    Opis:
    Cytosolic phospholipase A2 (cPLA2) preferentially liberates arachidonic acid (AA), which is known to be elevated in Alzheimer's disease (AD). The aim of this study was to investigate the possible relationship between enhanced nitric oxide (NO) generation observed in AD and cPLA2 protein level, phosphorylation, and AA release in rat pheochromocytoma cell lines (PC12) differing in amyloid beta secretion. PC12 control cells, PC12 cells bearing the Swedish double mutation in amyloid beta precursor protein (APPsw), and PC12 cells transfected with human APP (APPwt) were used. The transfected APPwt and APPsw PC12 cells showed an about 2.8- and 4.8-fold increase of amyloid β (Aβ) secretion comparing to control PC12 cells. An increase of NO synthase activity, cGMP and free radical levels in APPsw and APPwt PC12 cells was observed. cPLA2 protein level was higher in APPsw and APPwt PC12 cells comparing to PC12 cells. Moreover, phosphorylated cPLA2 protein level and [3H]AA release were also higher in APP-transfected PC12 cells than in the control PC12 cells. An NO donor, sodium nitroprusside, stimulated [3H]AA release from prelabeled cells. The highest NO-induced AA release was observed in control PC12 cells, the effect in the other cell lines being statistically insignificant. Inhibition of cPLA2 by AACOCF3 significantly decreased the AA release. Inhibitors of nNOS and γ-secretase reduced AA release in APPsw and APPwt PC12 cells. The basal cytosolic [Ca2+]i and mitochondrial Ca2+ concentration was not changed in all investigated cell lines. Stimulation with thapsigargin increased the cytosolic and mitochondrial Ca2+ level, activated NOS and stimulated AA release in APP-transfected PC12 cells. These results indicate that Aβ peptides enhance the protein level and phosphorylation of cPLA2 and AA release by the NO signaling pathway.
    Źródło:
    Acta Biochimica Polonica; 2007, 54, 3; 611-623
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-5 z 5

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