Temat: nitric oxide synthase - Katalog OPAC zbiorów

Skocz do pozycji: 1.

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

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Skocz do pozycji: 2.

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

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Skocz do pozycji: 3.

Tytuł:: Histochemical study of the nitric oxide synthase activity in experimental trichinellosis
Autorzy:: Hadas, E.
Gustowska, L.
Boczon, K.
Janczewska, D.
Powiązania:: https://bibliotekanauki.pl/articles/837102.pdf
Data publikacji:: 1998
Wydawca:: Polskie Towarzystwo Parazytologiczne
Tematy:: parasite
nitric oxide synthase
mouse
mice
trichinellosis
enzyme
nitric oxide
Trichinella spiralis
synthase activity
Źródło:: Annals of Parasitology; 1998, 44, 3
0043-5163
Pojawia się w:: Annals of Parasitology
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 4.

Tytuł:: Effect of oligochitosans on expression of inos gene in ehrlich ascites tumour in vitro
Autorzy:: Ignacak, Jan
Wiśniewska-Wrona, Maria
Dulińska-Litewka, Joanna
Pałka, Iwona
Zagajewski, Jacek
Niekraszewicz, Antoni
Powiązania:: https://bibliotekanauki.pl/articles/1035407.pdf
Data publikacji:: 2012
Wydawca:: Sieć Badawcza Łukasiewicz - Polskie Towarzystwo Chitynowe
Tematy:: chitosan oligomers
histone H1
iNOS (inducible nitric oxide synthase)
nitric oxide
Opis:: Oligochitosans obtained through degradation of macromolecules of chitosan with a high degree of deacetylation turned out to be biologically active, contributing to an increase of nitric oxide levels in Ehrlich ascites tumor (EAT) cells through inducing expression of the isoform of inducible nitric oxide synthase (iNOS) gene. An increase of NO levels in EAT cells in the presence of the investigated oligochitosans might contribute to nitrosylation of L-cysteine – an allosteric effector of the M2 isoenzyme of pyruvate kinase (PK), which switches the PK kinase activity, responsible for ATP synthesis, to the histone kinase activity that may participate in histone H1 phosphorylation. Lack of the histone activity of the PK M2 isoenzyme may contribute to decreased histone H1 phosphorylation and thus inhibit EAT cells proliferation.
Źródło:: Progress on Chemistry and Application of Chitin and its Derivatives; 2012, 17; 141-148
1896-5644
Pojawia się w:: Progress on Chemistry and Application of Chitin and its Derivatives
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 5.

Tytuł:: Nonsteroidal anti-inflammatory drugs impair oral mucosal repair by eliciting disturbances in endothelin-converting enzyme-1 and constitutive nitric oxide synthase
Autorzy:: Slomiany, B.L.
Slomiany, A.
Powiązania:: https://bibliotekanauki.pl/articles/69594.pdf
Data publikacji:: 2001
Wydawca:: Polskie Towarzystwo Fizjologiczne
Tematy:: nonsteroidal antiinflammatory drug
nitric oxide synthase
ulcer healing
oral mucosa
indomethacin
impairment
aspirin
apoptosis
Źródło:: Journal of Physiology and Pharmacology; 2001, 52, 1
0867-5910
Pojawia się w:: Journal of Physiology and Pharmacology
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 6.

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

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Skocz do pozycji: 7.

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

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Skocz do pozycji: 8.

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

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Skocz do pozycji: 9.

Tytuł:: Wpływ hiperoksji i hiperbarii na ekspresję białek szoku cieplnego i aktywność syntazy tlenku azotu – przegląd badań
The influence of hyperoxia on heat shock proteins expression and nitric oxide synthase activity – the review
Autorzy:: Szyller, J.
Kozakiewicz, M.
Siermontowski, P.
Powiązania:: https://bibliotekanauki.pl/articles/1359730.pdf
Data publikacji:: 2017
Wydawca:: Polskie Towarzystwo Medycyny i Techniki Hiperbarycznej
Tematy:: stres oksydacyjny
hiperoksja
hiperbaria
białka szoku cieplnego
syntaza tlenku azotu
oxidative stress
hyperoxia
hyperbaria
heat-shock proteins
nitric oxide synthase
Opis:: Przebywanie w środowisku o zwiększonej zawartości tlenu (wyższym ciśnieniu parcjalnym tlenu, pO2) i pod zwiększonym ciśnieniem (hiperbaria) prowadzi do nasilenia stresu oksydacyjnego. Reaktywne formy tlenu (ROS) uszkadzają cząsteczki białek, kwasów nukleinowych, powodują oksydację lipidów i zaangażowane są w rozwój wielu chorób m.in. układu krążenia, chorób neurodegeneracyjnych i in. Istnieją mechanizmy ochrony przed niekorzystnymi skutkami stresu oksydacyjnego. Należą do nich układy enzymatyczne i nieenzymatyczne. Do tych ostatnich zaliczają się m.in. białka szoku cieplnego (HSP). Dokładna ich rola i mechanizm działania są intensywnie badane w ostatnich latach. Hiperoksja i hiperbaria wpływa także na ekspresję i aktywność syntazy tlenku azotu (NOS). Jej produkt – tlenek azotu (NO) może reagować z reaktywnymi formami tlenu i przyczyniać się do rozwoju stresu nitrozacyjnego. NOS występuje w postaci izoform w różnych tkankach i w różny sposób reagujących na omawiane czynniki. Autorzy dokonali krótkiego przeglądu badań określających wpływ hiperoksji i hiperbarii na ekspresję HSP i aktywność NOS.
Any stay in an environment with an increased oxygen content (a higher oxygen partial pressure, pO2) and an increased pressure (hyperbaric conditions) leads to an intensification of oxidative stress. Reactive oxygen species (ROS) damage the molecules of proteins, nucleic acids, cause lipid oxidation and are engaged in the development of numerous diseases, including diseases of the circulatory system, neurodegenerative diseases, etc. There are certain mechanisms of protection against unfavourable effects of oxidative stress. Enzymatic and non-enzymatic systems belong to them. The latter include, among others, heat shock proteins (HSP). Their precise role and mechanism of action have been a subject of intensive research conducted in recent years. Hyperoxia and hyperbaria also have an effect on the expression and activity of nitrogen oxide synthase (NOS). Its product - nitrogen oxide (NO) can react with reactive oxygen species and contribute to the development of nitrosative stress. NOS occurs as isoforms in various tissues and exhibit different reactions to the discussed factors. The authors have prepared a brief review of research determining the effect of hyperoxia and hyperbaria on HSP expression and NOS activity.
Źródło:: Polish Hyperbaric Research; 2017, 1(58); 41-50
1734-7009
2084-0535
Pojawia się w:: Polish Hyperbaric Research
Dostawca treści:: Biblioteka Nauki