Showing papers in "Nitric Oxide in 1997"

TL;DR: Results reveal that peroxynitrite, hypochlorous acid, and H2O2 plus peroxidase all oxidize DCDHF and DHR to varying degrees but that neither superoxide, H2 O2 alone, nor physiological levels of nitric oxide are capable of indicator oxidation.

TL;DR: The current understanding of cytotoxic versus cytoprotective effects of NO in mammalian cells is reviewed and the janus-faced properties of this important small molecule are highlighted.

TL;DR: The results suggest that the actions of NO are surprisingly long range and the diffusion of NO is an important determinant of its biological actions.

TL;DR: The present paper overviews the various DNA modifications induced by exposure to peroxynitrite or NO and superoxide concurrently, with special reference to the formation of 8-nitroguanine and 8-oxoguanine as well as the induction of DNA single strand breakage.

TL;DR: Data indicate that substrate recognition differs markedly between the inducible L-arginine transporter hCAT-2B and the inroduible NOS II, with different L- arginine analogues having affinity to only one or both of these proteins.

TL;DR: Insights are provided into the role of NO in apoptotic signal transduction, with special regard to the Bcl-2 homologous proteins, the protease family of caspases and heat shock proteins.

TL;DR: Although all methods studied were suitable for quantifying end products of NO in biological fluids and media, the use of bacterial reductase and the modified Griess reaction proved successful to provide the greatest sensitivity and linear range for routine measurements of NO2- and NO3-.

TL;DR: Iron can induce both degradation and synthesis of S-nitrosothiols in the reaction system according to the proposed mechanisms such opposite effects of iron are determined by the ratio between S- nitrogen, thiols, iron, and NO in the Reaction system.

TL;DR: No produced by eNOS may be adequate to prevent necrosis by a mechanism independent of PMN, while induced NO appears to prevent apoptosis in LPS-treated rats receiving infusions of either NAME or NIL.

TL;DR: The results demonstrate the importance of NO delivery systems in the enhancement of cisplatin cytotoxicity and may provide insights into strategies for participation of NO donors and nitric oxide synthase with cisPlatin therapy.

TL;DR: The interaction between NOS2 and TGF-beta1 may represent a central homeostatic mechanism in mammalian physiology with implications for a variety of human diseases.

TL;DR: It is suggested that the cellular regulatory processes of NO to protect cells from apoptosis may be independent of the redox state and that low concentrations of NO and ONOO- inhibit the cellular suicide program in HUVEC via S-nitrosylation of members of the caspase family.

TL;DR: The ability of dopamine to increase 2',5'-cyclic adenosine monophosphate (cAMP) formation in cultured striatal neurons was blocked by its nitration by NO or its nitrogen oxide derivatives.

TL;DR: Nitric oxide-induced toxicity was investigated in two different cell lines, Chinese hamster ovary (CHO-AA8) and human lymphoblastoid (TK6), over a range of NO doses to indicate that NO.-induced toxicity is an extremely complex process involving multiple pathways generally leading to apoptotic cell death.

TL;DR: The enzymatic synthesis of NO from L-arginine by endothelial NOS appears to be partially regulated by binding of both calmodulin and substrate, a significant departure from the enzymatics properties of the other constitutive NOS isoform, neuronal NOS, and the physiological implications are interpreted.

TL;DR: It is demonstrated that hyperthyroidism leads to a significant and reversible enhancement in rat liver NOS activity, an effect that is exerted at hepatocyte and Kupffer cell levels, thus representing an additional source of prooxidants to those of reactive oxygen species.

TL;DR: Hydroxylamines TEMPONE-H and CP-H can be used as nontoxic compounds in ESR assay capable of quantifying the formation of superoxide radicals and peroxynitrite in suspensions of cells and in the whole blood with high sensitivity.

TL;DR: The increase in cGMP induced by NO stimulation of the guanylyl cyclase decreases the exocytotic release of glutamate, but higher NO levels reduce the ATP/ADP ratio by inhibiting mitochondrial function, which therefore causes the massive release of cytosolic glutamate through the glutamate carrier.

TL;DR: Rat C6 glioma cells were stably transfected with a human cDNA encoding heat shock protein (HSP) 70 to demonstrate that constitutive HSP70 expression in glial cells can reduce NOS-2 induction, presumably due to inhibition of NFκB nuclear uptake.

TL;DR: DCFH is a useful probe for quantitation of NOS-2 activity in activated rat lung macrophages and a strong correlation in DCFH oxidation with nitrite production in the same samples was found.

TL;DR: Results are suggestive of a role for monocytic iNOS in the autoimmune response underlying the pathogenesis of multiple sclerosis.

TL;DR: Changes in flavin and protein fluorescence of neuronal nitric oxide synthase (nNOS) and its flavoprotein module were studied in the presence of urea and compared with those previously reported for cytochrome P450 reductase (CPR).

TL;DR: Some biological actions of DDC may result from SNO elimination rather than SOD inactivation, and apparent DDC-induced potentiation of superoxide effects may derive from O2- produced during the conversion of SNO to NO.

TL;DR: This work probed the reaction of peroxynitrite with a limiting amount of CO2 at pH 7.4 and 25 degrees C in the presence of tyrosine and suggested that tyrosines partially traps intermediates that arise from the CO2-peroxysitrite reaction, causing the fraction of theCO2 that recycles to decrease and the lifetime of per oxynitrites to increase.

TL;DR: No is partially responsible for the detrimental effect of TNF-alpha on BBB function, and the mechanism of NO-induced barrier dysfunction does not involve an inhibition of endothelial mitochondrial electron transport chain and reduced energy resources.

TL;DR: When tested on some cloned rat 5-HT receptors stably transfected into LMTK- cells, both 4-nitroso and 4-Nitro derivatives behaved as agonists and antagonists toward 5-ht1B and 5- HT2B receptors, respectively.

TL;DR: The sparing of epithelial cells while compromising the viability of macrophages suggests that PHY may be beneficial in autoimmune disorders.

TL;DR: The reagents capable of effecting electrophilic and free radical nitrosation are briefly reviewed, together with the appropriate mechanisms, and in the light of these findings the possibilities of peroxynitrite/peroxyn itrous acid acting as a nitrosating species are considered.

TL;DR: The results suggest that NO is spontaneously produced in the corneal endothelium and the NO/cyclic GMP pathway is involved in maintainance of cornesal thickness.

TL;DR: Findings suggest that ferritin induction, presumably via release of nitric oxide, may be a mechanism underlying long-term cytoprotection by SIN-1 against oxidative stress.