Showing papers in "Nitric Oxide in 2005"

TL;DR: The data demonstrate that the accumulation of nitrosyl-iron complexes reflects a sharp rise in endogenous NO production inside the affected tissue, and the beneficial action of the treatment is attributed to enhanced NO bioavailability.

TL;DR: The results suggest that NO can effectively protect plants from UV-B damage mostly probably mediated by enhanced activities of antioxidant enzymes.

TL;DR: The present results indicate that the molecular mechanism of clinically observed anti-inflammatory action of ESW should include tyrosine-dephosphorylation of eNOS, a successive increase in NO production and suppression of NF-kappaB activation.

TL;DR: The increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.

TL;DR: Administration of NO in experimental stroke reduces stroke lesion volume in permanent and transient models and support clinical trials in stroke patients, although the presence of a narrow therapeutic time window may be a limiting factor.

TL;DR: A consistent difference in the distribution of eNOS genetic variants in blacks compared with whites is strongly suggested and indicates that the interethnic differences do not vary with geographic origin.

TL;DR: It is shown that human faeces can generate NO after nitrate or nitrite supplementation, and it is concluded that NO can be generated by the anaerobic gut flora in the presence of nitrateor nitrite.

TL;DR: The designed gNO exposure system is capable of supporting cellular viability for a representative range of prokaryote and eukaryotic cells and is also capable of obtaining toxicological data.

TL;DR: An improved method allowing the above limitation to be erased is laid out, using sulfamic acid for nitrite removal and some modifications that enhance the reproducibility of the assay are described.

TL;DR: In this article, the inflammatory response of Raw 264.7 macrophages to bacterial lipopolysaccharide (LPS) by assessment of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression was found to be attenuated by both isothiocyanates (ITCs) in a concentration-dependent manner.

TL;DR: Administration of a selective iNOS inhibitor, 1400W, even delayed by 18 h improves histopathological outcome supporting a detrimental role for iN OS induction after TBI.

TL;DR: The results indicate multiple unique proteins not previously identified as S-nitrosylation targets: enolase, pyruvate kinase, elongation factor-1 and -2, plastin-2, FRAG-6, CEM-16, and SMC-6.

TL;DR: There is a reciprocal cross-talk between inductions of HO-1 and iNOS in macrophages stimulated with LPS leading to their survival, and this appears to be related to the role of redox-sensitive transcription factor Nrf2 in the nuclear protein fraction.

TL;DR: It is suggested that l-arginine attenuates APE-induced pulmonary hypertension through antioxidant mechanisms involving increased NO synthesis, and blunted the increase in TBA-RS observed after APE.

TL;DR: It is concluded that CIO triggers liver oxidative stress at early times, with upregulation of iNOS expression involving the ERK/NF-kappaB pathway at later times, a finding that may represent a hepatoprotective mechanism against CIO toxicity in addition to the recovery of GSH homeostasis.

TL;DR: Interestingly, activation of Nos2-reporter gene constructs containing the proximal 188 bp or proximal 94 bp of the rat promoter also was inhibited with the same rank order of potency, while low concentrations of helenalin increased activity of both promoter constructs, while BAY 11-7082 poorly inhibited the 94-bp activity.

TL;DR: Surprisingly, in nNOS-/--mice the skeletal muscle showed patterns of significant nNos-immunoreactivity and NADPH-d activity possibly due to alternative nN OS-splice isoforms, which might be up-regulated to compensate for decreased NO formation.

TL;DR: It is clear that ONO(2)(-) can react with the protein moieties of the enzymes, and derivatizes a select few tyrosine residues in both complexes I and III forming 3-nitrotyrosine as detected by immunoblots.

TL;DR: It is suggested that T-786C and C774T eNOS polymorphisms affect the onset pattern of severe DR, supported by previous associations between eN OS4b/a polymorphism and DR.

TL;DR: It is concluded that not only acute hypobaric hypoxia but also either hypobaria orhypoxia alone induce changes in NOx serum levels, which involve a decrease in NOxs, greater and longer-lasting in hypoxIA alone than in hypOBaria and Hypoxia together.

TL;DR: In this article, the effects of water extract of Korea red ginseng (KRG) on NO concentration levels in the exhaled breath, blood pressure, and heart rate of human volunteers were investigated.

TL;DR: It is proposed that these mechanisms of TGF-β1 in the posttranslational regulation of iNOS gene expression may contribute to suppression of excess nitric oxide during inflammatory processes.

TL;DR: The results clearly demonstrated that NO+ rapidly and drastically decrease the amount of glucose in mung bean leaves, and suggested that chloroplasts might be one of the main sub-cellular targets of NO in plants.

TL;DR: The 3-NT levels were much lower compared to previously reported levels, based on immunochemical measurements, and the method does not allow the simultaneous quantification of tyrosine in samples.

TL;DR: The data suggest that bacterial nitric oxide synthases may, at least in part, produce NO for biosynthetic purposes, rather than for cellular signaling, as they do in mammals.

TL;DR: There does not appear to be a profound effect of the primary sequence of adjacent amino acid residues on the rate of cysteine S-nitrosylation at least at the peptide levels, and this data validate the importance of Cys98 in regulating eNOS dimerization and activity, and the utility of mass spectroscopy to identify Cysteine residues susceptible to S-Nitrosoylation.

TL;DR: It is suggested that EFS induces a similar nNOS-derived NO release in segments from orchidectomized and control male rats, despite the decrease in nN OS expression in orchidECTomized rats.

TL;DR: The implication of these findings is that MPO acts as gatekeeper, suppressing the deleterious induction of iNOS at inflammatory sites by illegitimate signals, as the combined signaling of IFNgamma/LPS overrides the gatekeeper function by suppressing MPO gene expression.

TL;DR: It is concluded that yeasts induced augmented NO production in C. megacephala hemolymph and granular cells are the hemocyte type involved with the generation of this molecule.

TL;DR: The results suggest that iNOS expression in bladder tissue may predispose to cancer recurrences and high urine NO levels could be generated by an active iN OS present not only in the tumor but also in the non-tumoral bladder tissue.