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Tytuł:
Cytotoxic effect of nitric oxide on human hematological malignant cells.
Autorzy:
Tsumori, Michihiro
Tanaka, Junko
Koshimura, Kunio
Kawaguchi, Mikiko
Murakami, Yoshio
Kato, Yuzuru
Powiązania:
https://bibliotekanauki.pl/articles/1043819.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
lymphoma
myeloma
leukemia
nitric oxide
Opis:
We investigated the cytotoxic effect of nitric oxide (NO) on primary culture of human hematological malignant cells. Sodium nitroprusside (SNP), an NO donor, had cytotoxic effects on the cells of some patients with malignant lymphoma (ML), acute myelocytic leukemia (AML) or chronic myelomonocytic leukemia (CMMoL), but not with multiple myeloma. Cultured cells from the ML patient remained sensitive to SNP after the cells became resistant to anti-cancer drugs. In contrast, the cells from the patients with AML and CMMoL became resistant to SNP while anti-cancer drugs remained effective. In samples of the cells of the patients with ML and AML, the number of CD3 positive lymphoma cell was decreased by SNP and the number of CD33 negative cells and normal B lymphocytes (CD19 positive cells) were increased. In the cells of the patient with ML, apoptosis was induced by SNP. SNP had no effect on lymphocytes of healthy volunteers. These results suggest that SNP had an anti-tumor effect on human hematological malignant cells.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 139-144
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
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:
Nitric oxide and platelet energy metabolism.
Autorzy:
Tomasiak, Marian
Stelmach, Halina
Rusak, Tomasz
Wysocka, Jolanta
Powiązania:
https://bibliotekanauki.pl/articles/1041559.pdf
Data publikacji:
2004
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
mitochondrial energy production
porcine platelets
nitric oxide
glycolysis
Opis:
This study was undertaken to determine whether nitric oxide (NO) can affect platelet responses through the inhibition of energy production. It was found that NO donors: S-nitroso-N-acetylpenicyllamine, SNAP, (5-50 μM) and sodium nitroprusside, SNP, (5-100 μM) inhibited collagen- and ADP-induced aggregation of porcine platelets. The corresponding IC50 values for SNAP and SNP varied from 5 to 30 μM and from 9 to 75 μM, respectively. Collagen- and thrombin-induced platelet secretion was inhibited by SNAP (IC50 = 50 μM) and by SNP (IC50 = 100 μM). SNAP (20-100 μM), SNP (10-200 μM) and collagen (20 μg/ml) stimulated glycolysis in intact platelets. The degree of glycolysis stimulation exerted by NO donors was similar to that produced by respiratory chain inhibitors (cyanide and antimycin A) or uncouplers (2,4-dinitrophenol). Neither the NO donors nor the respiratory chain blockers affected glycolysis in platelet homogenate. SNAP (20-100 μM) and SNP (50-200 μM) inhibited oxygen consumption by platelets. The effect of SNP and SNAP on glycolysis and respiration was not reduced by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one, a selective inhibitor of NO-stimulated guanylate cyclase. SNAP (5-100 μM) and SNP (10-300 μM) inhibited the activity of platelet cytochrome oxidase and had no effect on NADH:ubiquinone oxidoreductase and succinate dehydrogenase. Blocking of the mitochondrial energy production by antimycin A slightly affected collagen-evoked aggregation and strongly inhibited platelet secretion. The results indicate that: 1) in porcine platelets NO is able to diminish mitochondrial energy production through the inhibition of cytochrome oxidase, 2) the inhibitory effect of NO on platelet secretion (but not aggregation) can be attributed to the reduction of mitochondrial energy production.
Źródło:
Acta Biochimica Polonica; 2004, 51, 3; 789-803
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Monitoring of urine nitric oxide (NO) related substrates and immunological competence in hematological malignancy.
Autorzy:
Tanaka, Junko
Koshimura, Kunio
Tsumori, Michihiro
Murakami, Yoshio
Kato, Yuzuru
Powiązania:
https://bibliotekanauki.pl/articles/1043832.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
pokeweed mitogen
hematological malignancy
urine nitric oxide
phytohemagglutinin
Opis:
It has been reported that concentrations of neopterin in the urine are changed according to the host immunological conditions. In the present study, we measured urinary concentration of neopterin in patients with malignant hematological disorders and investigated the relationship between urinary neopterin levels and laboratory indices for cellular immunity. Urine neopterin levels were correlated with serum sIL-2R levels in the patients with malignant lymphoma, and inversely correlated with lymphocyte reactivity with ConA in the patients with acute myelocytic leukemia. However, no significant correlation was observed between urine neopterin levels and lymphocyte reactivity with phytohemagglutinin and pokeweed mitogen, CD4/8 ratio, CD56+16+ subset or serum IFN-β levels. In the patients with malignant lymphoma, parallel changes in serum sIL-2R and urine neopterin were observed. The presented results suggest that urine neopterin levels are related to the activation of T cells in malignant lymphoma.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 227-232
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:
Mitochondria recycle nitrite back to the bioregulator nitric monoxide.
Autorzy:
Nohl, Hans
Staniek, Katrin
Sobhian, Babak
Bahrami, Soheyl
Redl, Heinz
Kozlov, Andrey
Powiązania:
https://bibliotekanauki.pl/articles/1044210.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
nitrite reductase
electron paramagnetic resonance
nitric oxide
mitochondria
Opis:
Nitric monoxide (NO) exerts a great variety of physiological functions. L-Arginine supplies amino groups which are transformed to NO in various NO-synthase-active isoenzyme complexes. NO-synthesis is stimulated under various conditions increasing the tissue of stable NO-metabolites. The major oxidation product found is nitrite. Elevated nitrite levels were reported to exist in a variety of diseases including HIV, reperfusion injury and hypovolemic shock. Denitrifying bacteria such as Paracoccus denitrificans have a membrane bound set of cytochromes (cyt cd1, cyt bc) which were shown to be involved in nitrite reduction activities. Mammalian mitochondria have similar cytochromes which form part of the respiratory chain. Like in bacteria quinols are used as reductants of these types of cytochromes. The observation of one-e- divergence from this redox-couple to external dioxygen made us to study whether this site of the respiratory chain may also recycle nitrite back to its bioactive form NO. Thus, the aim of the present study was therefore to confirm the existence of a reductive pathway which reestablishes the existence of the bioregulator NO from its main metabolite NO2-. Our results show that respiring mitochondria readily reduce added nitrite to NO which was made visible by nitrosylation of deoxyhemoglobin. The adduct gives characteristic triplet-ESR-signals. Using inhibitors of the respiratory chain for chemical sequestration of respiratory segments we were able to identify the site where nitrite is reduced. The results confirm the ubiquinone/cyt bc1 couple as the reductant site where nitrite is recycled. The high affinity of NO to the heme-iron of cytochrome oxidase will result in an impairment of mitochondrial energy-production. "Nitrite tolerance" of angina pectoris patients using NO-donors may be explained in that way.
Źródło:
Acta Biochimica Polonica; 2000, 47, 4; 913-921
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Exogenous nitric oxide inhibits shedding of ADAM17 substrates
Autorzy:
Bzowska, Monika
Stalińska, Krystyna
Mężyk-Kopeć, Renata
Wawro, Karolina
Duda, Katarzyna
Das, Sudipta
Bereta, Joanna
Powiązania:
https://bibliotekanauki.pl/articles/1040593.pdf
Data publikacji:
2009
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
shedding
ADAM17
TNF receptor 1
TNF
nitric oxide
Opis:
Both ADAM17, the secretase responsible for the shedding of ectodomains of numerous membrane proteins including TNF and its receptors, as well as nitric oxide synthesized by inducible nitric oxide synthase play regulatory roles in inflammation and tumor progression. We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. We found that endogenous nitric oxide influenced neither ADAM17 mRNA level nor the shedding of two ADAM17 substrates, TNF and TNFR1. Exogenous NO significantly diminished the release of TNF and TNFR1 without affecting the ADAM17 transcript level. Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). We discuss potential mechanisms of NO-mediated inhibition of ectodomain shedding and possible reasons of discrepancy between our results and the previous report.
Źródło:
Acta Biochimica Polonica; 2009, 56, 2; 325-335
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Antioxidant properties of PF9601N, a novel MAO-B inhibitor: assessment of its ability to interact with reactive nitrogen species
Autorzy:
Bellik, Lydia
Dragoni, Stefania
Pessina, Federica
Sanz, Elisenda
Unzeta, Mercedes
Valoti, Massimo
Powiązania:
https://bibliotekanauki.pl/articles/1040409.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
MAO-B inhibitors
peroxynitrite
l-deprenyl
nitric oxide
Parkinson's disease
Opis:
The novel MAO-B inhibitor PF9601N, its cytochrome P450-dependent metabolite FA72 and l-deprenyl were studied as potential peroxynitrite (ONOO-) scavengers and nitric oxide synthase (NOS) inhibitors. The scavenging activity of these compounds was evaluated by measuring the oxygen consumption through peroxynitrite-mediated oxidation of both linoleic acid and brain homogenate. FA72, PF9601N and l-deprenyl caused a concentration-dependent inhibition of ONOO--induced linoleic acid oxidation with an IC50 value of 60.2 µM, 82.8 µM and 235.8 µM, respectively. FA72 was the most potent also in inhibiting ONOO--induced brain homogenate oxidation with an IC50 value of 99.4 µM, while PF9601N and l-deprenyl resulted weaker inhibitors in the same experimental model, showing an IC50 value of 164.8 and 112.0 µM, respectively. Furthermore, both the novel MAO-B inhibitor as well as its metabolite were able to strongly inhibit rat brain neuronal NOS (IC50 of 183 µM and 192 µM, respectively), while l-deprenyl at the highest concentration used (3 mM), caused only a slight decrease of the enzyme activity. Moreover, inducible NOS was strongly inhibited by FA72 only. All these results suggest that PF9601N could be a promising therapeutic agent in neurodegenerative disorders such as Parkinson's disease.
Źródło:
Acta Biochimica Polonica; 2010, 57, 2; 235-239
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Carbon monoxide - a "new" gaseous modulator of gene expression.
Autorzy:
Dulak, Józef
Józkowicz, Alicja
Powiązania:
https://bibliotekanauki.pl/articles/1043644.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
angiogenesis
vascular endothelial growth factor
atherosclerosis
nitric oxide
oxidative stress
Opis:
Carbon monoxide (CO) is an odorless, tasteless and colorless gas which is generated by heme oxygenase enzymes (HOs). HOs degrade heme releasing equimolar amounts of CO, iron and biliverdin, which is subsequently reduced to bilirubin. CO shares many properties with nitric oxide (NO), an established cellular messenger. Both CO and NO are involved in neural transmission and modulation of blood vessel function, including their relaxation and inhibition of platelet aggregation. CO, like NO, binds to heme proteins, although CO binds only ferrous (FeII) heme, whereas NO binds both ferrous and ferric (FeIII). CO enhances the activity of guanylate cyclase although it is less potent than NO. In contrast, CO inhibits other heme proteins, such as catalase or cytochrome P450. The effects of CO on gene expression can be thus varied, depending on the cellular microenvironment and the metabolic pathway being influenced. In this review the regulation of gene expression by HO/CO in the cardiovascular system is discussed. Recent data, derived also from our studies, indicate that HO/CO are significant modulators of inflammatory reactions, influencing the underlying processes such as cell proliferation and production of cytokines and growth factors.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 31-47
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of cyclosporin A on immunological response in lungs of guinea pigs infected with Trichinella spiralis.
Autorzy:
Dzik, Jolanta
Zieliński, Zbigniew
Gołos, Barbara
Jagielska, Elżbieta
Wranicz, Mariusz
Wałajtys-Rode, Elżbieta
Powiązania:
https://bibliotekanauki.pl/articles/1043834.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
bronchoalveolar lavage
cyclosporin A
Trichinella
lungs
trichinellosis
nitric oxide
superoxide
Opis:
The effects of cyclosporin A (CsA), a potent immunosuppressive drug with antiparasitic activity, on the innate immunological response in guinea pig lungs during an early period (6th and 14th days) after T. spiralis infection were studied. CsA treatment of T. spiralis-infected guinea pigs caused a significant attenuation of immunological response in lungs by decreasing lymphocyte infiltration into pulmonary alveolar space, inhibiting alveolar macrophage superoxide anion production and lowering both the production of NO metabolites measured in bronchoalveolar lavage fluid and expression of the iNOS protein in lung homogenates, allowing us to speculate that the T. spiralis-dependent immunological response is dependent on lymphocyte T function. Interestingly, CsA itself had a pro-inflammatory effect, promoting leucocyte accumulation and macrophage superoxide production in guinea pig lungs. This observation may have a relevance to the situation in patients undergoing CsA therapy. Macrophage expression of the iNOS protein, evaluated by immunoblotting was not influenced by treatment of animals with CsA or anti-TGF-antibody, indicating different regulation of the guinea pig and murine enzymes.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 233-247
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Molecular mechanism of PC12 cell death evoked by sodium nitroprusside, a nitric oxide donor
Autorzy:
Pytlowany, Magdalena
Strosznajder, Joanna
Jęśko, Henryk
Cąkała, Magdalena
Strosznajder, Robert
Powiązania:
https://bibliotekanauki.pl/articles/1040752.pdf
Data publikacji:
2008
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
nitric oxide
apoptosis-inducing factor
PC12
cell death
lipoxygenase
cyclooxygenase
Opis:
Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (AA), a substrate for cyclo- and lipoxygenases (COX and LOX, respectively). In this study we investigated biochemical processes leading to cell death evoked by an NO donor, sodium nitroprusside (SNP). We found that SNP decreased viability of pheochromocytoma (PC12) cells in a concentration- and time-dependent manner. SNP at 0.1 mM caused a significant increase of apoptosis-inducing factor (AIF) protein level in mitochondria. Under these conditions 80% of PC12 cells survived. The enhancement of mitochondrial AIF level might protect most of PC12 cells against death. However, NO released from 0.5 mM SNP induced massive cell death but had no effect on protein level and localization of AIF and cytochrome c. Caspase-3 activity and poly(ADP-ribose) polymerase-1 (PARP-1) protein levels were not changed. However, PARP activity significantly decreased in a time-dependent manner. Inhibition of both COX isoforms and of 12/15-LOX significantly lowered the SNP-evoked cell death. We conclude that AIF, cytochrome c and caspase-3 are not responsible for the NO-mediated cell death evoked by SNP. The data demonstrate that NO liberated in excess decreases PARP-1 activity. Our results indicate that COX(s) and LOX(s) are involved in PC12 cell death evoked by NO released from its donor, SNP.
Źródło:
Acta Biochimica Polonica; 2008, 55, 2; 339-347
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Endothelial NADH/NADPH-dependent enzymatic sources of superoxide production: relationship to endothelial dysfunction.
Autorzy:
Kalinowski, Leszek
Malinski, Tadeusz
Powiązania:
https://bibliotekanauki.pl/articles/1043282.pdf
Data publikacji:
2004
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
peroxynitrite
endothelial dysfunction
NAD(P)H oxidase
nitric oxide
superoxide
eNOS
Opis:
There is growing evidence that endothelial dysfunction, which is often defined as the decreased endothelial-derived nitric oxide (NO) bioavailability, is a crucial factor leading to vascular disease states such as hypertension, diabetes, atherosclerosis, heart failure and cigarette smoking. This is due to the fact that the lack of NO in endothelium-dependent vascular disorders contributes to impaired vascular relaxation, platelet aggregation, increased vascular smooth muscle proliferation, and enhanced leukocyte adhesion to the endothelium. During the last several years, it has become clear that reduction of NO bioavailability in the endothelium-impaired function disorders is associated with an increase in endothelial production of superoxide (O2̇̄). Because O2̇̄ rapidly scavenges NO within the endothelium, a reduction of bioactive NO might occur despite an increased NO generation. Among many enzymatic systems that are capable of producing O2̇̄, NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O2̇̄ in the endothelial cells. It seems that O2̇̄ generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O2̇̄. That is maintained at diverse levels.
Źródło:
Acta Biochimica Polonica; 2004, 51, 2; 459-469
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effects of protoporphyrins on production of nitric oxide and expression of vascular endothelial growth factor in vascular smooth muscle cells and macrophages.
Autorzy:
Józkowicz, Alicja
Dulak, Józef
Powiązania:
https://bibliotekanauki.pl/articles/1043649.pdf
Data publikacji:
2003
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cell viability
metalloporphyrins
vascular endothelial growth factor
nitric oxide
heme oxygenase
Opis:
Heme oxygenase-1 (HO-1), an inducible enzyme degrading heme to biliverdin, iron and carbon monoxide, is involved in regulation of inflammation and angiogenesis. Tin protoporphyrin (SnPPIX) and zinc protoporphyrin (ZnPPIX) are commonly used as competitive inhibitors of HO-1. We aimed to compare the effects of SnPPIX and ZnPPIX on the production of vascular endothelial growth factor (VEGF), activity of inducible nitric oxide synthase (iNOS) and cell viability. All experiments were performed on rat vascular smooth muscle cells and murine RAW264.7 macrophages treated with 3-10 μM protoporphyrins. Some cells were additionally stimulated with IL-1β or with lipopolysaccharide. After a 24 h incubation period SnPPIX and ZnPPIX significantly reduced the generation of VEGF in vascular smooth muscle cells and RAW264.7, both in resting and stimulated cells. The inhibitory potentials of both protoporphyrins on VEGF synthesis were very similar. In contrast, analysis of iNOS activity revealed that results obtained with different HO-1 inhibitors are discrepant. Generation of nitric oxide by iNOS was significantly increased by SnPPIX but strongly decreased by ZnPPIX. Similar differences were observed when cell viability was compared. SnPPIX improved the cell survival rate, whereas the same doses of ZnPPIX exerted some cytotoxic effects. In summary, SnPPIX and ZnPPIX can be used as HO-1 inhibitors in some experimental models. However, these compounds produce also HO-independent effects, which can make the interpretation of experiments very uncertain. Thus the involvement of the HO-1 pathway should be always confirmed by more specific methods.
Źródło:
Acta Biochimica Polonica; 2003, 50, 1; 69-79
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of Medicago sativa Mhb1gene expression on defense response of Arabidopsis thaliana plants
Autorzy:
Maassen, Anna
Hennig, Jacek
Powiązania:
https://bibliotekanauki.pl/articles/1039900.pdf
Data publikacji:
2011
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
Arabidopsis thaliana
pathogen infection
nitrotyrosine
nitric oxide
peroxidase activity
non-symbiotic hemoglobin
Opis:
Besides the previously described nitric oxide-detoxification activity we identified new features of class-1 non-symbiotic hemoglobin from Medicago sativa (Mhb1). Under in vitro conditions, using peroxidase in-gel activity assay, the Mhb1 protein was shown to possess also peroxidase-like activity. Due to this activity, in the presence of nitrite and hydrogen peroxide, the protein can mediate autonitration and nitration of other proteins at tyrosine residues, as revealed by tandem mass spectrometry and immune assay approaches. Mhb1 through its multifunctional activities can affect different components of signal transduction cascades operating during plant response to infections. This influence is manifested by Mhb1-mediated selective up-regulation of expression of certain pathogen inducible genes in Pseudomonas syringae infected Arabidopsis thaliana plants which overproduce Mhb1, as revealed by reverse transcription-quantitative real-time PCR analysis. Changes in expression level of these genes can influence such processes as synthesis of secondary metabolites, protein degradation and biosynthesis of ethylene. They can also result in alteration of pathogen-induced defense response of Mhb1 transgenic plants.
Źródło:
Acta Biochimica Polonica; 2011, 58, 3; 427-432
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

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