Disease relevance of S-Nitrosocysteine

• Specifically, we demonstrate that S-nitrosocysteinyl glycine (CGSNO) and S-nitroso-l-cysteine (l-CSNO)-but not S-nitroso-d-cysteine (d-CSNO)-reproduce the ventilatory effects of hypoxia at the level of the nucleus tractus solitarius (NTS) [1].
• In intact B16 melanoma cells treated with S-nitrosocysteine a rapid decrease in PKC activity in both cytosol and membrane was observed [2].
• RESULTS: In comparison with controls, rats with acute peritonitis were characterized by inflammatory changes, increased S-nitrosocysteine immunoreactivity, and increased NOS activities in the peritoneum, due to the up-regulation of endothelial and inducible NOS [3].
• Indirect evidence for nitric oxide involvement in multiple sclerosis by characterization of circulating antibodies directed against conjugated S-nitrosocysteine [4].
• MATERIALS AND METHODS: Murine T cell lymphoma EL4-6.1 cells were activated with the physiological stimulus interleukin (IL)-1beta to express IL-2 mRNA in the presence or absence of subtoxic concentrations of the physiological spontaneous NO donor S-nitrosocysteine (SNOC) [5].

Psychiatry related information on S-Nitrosocysteine

• Using Western blot analysis and quantitative immunofluorescent staining study, we found that water deprivation in rats significantly enhanced the expression of nitrosocysteine protein in SON and neural lobes [6].

High impact information on S-Nitrosocysteine

• Nitric oxide release from cultured bovine aortic endothelial cells was detected by chemiluminescence and bioassay experiments compared the vasodilator potencies of nitric oxide, S-nitrosocysteine, and EDRF [7].
• The current could also be activated by a phosphodiesterase inhibitor and the nitric oxide donors sodium nitroprusside and S-nitrosocysteine [8].
• Identification of S-nitrosylation motifs by site-specific mapping of the S-nitrosocysteine proteome in human vascular smooth muscle cells [9].
• Sequence analysis of the S-nitrosocysteine-containing peptides revealed the presence of acid/base motifs, as well as hydrophobic motifs surrounding the identified cysteine residues [9].
• Therefore, we used a proteomic approach using selective peptide capturing and site-specific adduct mapping to identify the targets of S-nitrosylation in human aortic smooth muscle cells upon exposure to S-nitrosocysteine and propylamine propylamine NONOate [9].

Chemical compound and disease context of S-Nitrosocysteine

• In rats with a hypersensitivity state following peripheral nerve injury, spinal administration of an NO donor or l-cysteine alone produced no effect, whereas their combination, which yields s-nitroso-l-cysteine (SNC) powerfully reduced hypersensitivity [10].
• Dopamine or SKF38393 (D1 receptor agonist) inhibited ionomycin (calcium ionophore)-induced toxicity, while dopamine did not affect S-nitrosocysteine (NO donor)-induced toxicity [11].
• Unilateral microinjection of L-glutamate into the nucleus tractus solitarii of conscious rats increased arterial pressure and caused bradycardia while microinjection of S-nitrosocysteine into the same site of these animals caused hypotension and bradycardia [12].

Biological context of S-Nitrosocysteine

• Cells were exposed to (1) S-nitrosocysteine (SNOC; 30 mumol/L) to induce nitric oxide-induced oxidative injury and (2) staurosporine (0.03 mumol/L) to induce apoptotic cell death [13].
• Treatment with 100 microM S-nitrosocysteine induced apoptosis of cerebellar neurons as indicated by nuclear condensation and phosphatidylserine exposure to the exoplasmic leaflet of the plasma membrane [14].
• In [Ca2+]i fluorimetric experiments on cultured hippocampal neurons, the nitric oxide-releasing agent S-nitrosocysteine produced a delayed rise in [Ca2+]i over a 20-min exposure, which was accompanied by a progressive slowing of the kinetics of recovery from depolarization-induced [Ca2+]i transients [15].
• Redox regulation of S-nitrosocysteine-mediated vasodilation in vivo [16].
• We examined the effects of intracisternal (i.c.) injections (10-250 nmol) of the L- and D-isomers of S-nitrosocysteine (L- and D-S-nitrosocysteine) on the mean arterial blood pressure and heart rate of conscious rats, and the decomposition of L- and D-S-nitrosocysteine to nitric oxide (NO) upon addition to brain homogenates [17].

Anatomical context of S-Nitrosocysteine

• Modulation of baroreceptor activity by nitric oxide and S-nitrosocysteine [18].
• The goal of this study was to determine whether nitric oxide (NO) and the NO donor, S-nitrosocysteine (cysNO), modulate the activity of carotid sinus baroreceptors [18].
• The NO donor S-nitrosocysteine induced a rapid transnitrosation reaction with hemoglobin in rat erythrocytes producing high levels of S-nitrosohemoglobin; this reaction in human red blood cells was negligible [19].
• We investigated the effect of S-nitroso-L-cysteine (SNC) on noradrenaline (NA) release in the rat hippocampus in vivo and in vitro [20].
• In parallel, peritoneal NOS enzymatic activities were measured and expression studies for NOS isoforms and S-nitrosocysteine reactivity performed in the peritoneum [3].

Associations of S-Nitrosocysteine with other chemical compounds

• Nitroglycerin dilates large (greater than or equal to 100 microns) but not small coronary arterial microvessels, and a putative metabolite of nitroglycerin, S-nitroso-L-cysteine, has been shown in vitro to dilate both large and small coronary microvessels [21].
• Pretreatment of RPASMs with H2O2 attenuated the untreated CPAE-induced, the putative EDRF S-nitroso-L-cysteine-induced, or the nitroprusside-induced increases in RPASM cGMP levels [22].
• Although the S-nitrosylcysteine adduct in hAGT is readily reversible by reaction with other cellular thiols, the formation of S-nitrosocysteine at Cys-145 was found to lead to the rapid degradation of the hAGT protein in vivo [23].
• The results evidenced that S-nitrosoglutathione is formed in erythrocytes treated with S-nitrosocysteine, a transnitrosating agent [24].
• The modulation of large conductance Ca2+-activated K+ (BKCa) channels by the nitric oxide (NO) donors S-nitroso-L-cysteine (NOCys) and sodium nitroprusside (SNP) and agents which oxidize or reduce reactive thiol groups were compared in excised inside-out membrane patches of the guinea-pig taenia caeci [25].

Gene context of S-Nitrosocysteine

• Identification of stereoselective transporters for S-nitroso-L-cysteine: role of LAT1 and LAT2 in biological activity of S-nitrosothiols [26].
• We observed that both S-nitrosocysteine and cytokine-activated NOS2 inhibited NF-kappaB in human respiratory cells or murine macrophages [27].
• 7. Exposure of vascular smooth muscle cells to either S-nitroso-L-cysteine (Cys-SNO, 10(-4) M), SNP (10(-4) M) or SIN-1 (10(-4) M) for 35 min affected minimally the basal activation of NF-kappa B but abolished that evoked by IL-1 beta (30 u ml-1 added during the last 30 min) [28].
• We also show that the modification occurs in endothelial cells when they are treated with S-nitroso-l-cysteine and when they are exposed to eNOS activators [29].
• We postulated that MS patients would exhibit an antibody (Ab) response directed against proteins containing S-nitrosocysteine (SNO-cysteine) and showed that anti-NO-cysteine Abs of the IgM isotype are in fact present in the sera of some MS patients (Boullerne et al., 1995) [30].

Analytical, diagnostic and therapeutic context of S-Nitrosocysteine

• The results of UV-vis and circular dichroism absorption, intrinsic fluorescence, and mass spectrometry measurements indicate that both Ca(2+)-loaded (holo) and Ca(2+)-free (apo) rHCaBP are S-nitrosated by S-nitrosocysteine (CysNO) [31].
• Electrospray ionization mass spectrometry was used to monitor the results of exposure of haemolysates to S-nitrosocysteine under different conditions and thus addressed some aspects of NO-haemoglobin interaction [32].
• The responses to S-nitrosocysteine were blocked by prior microinjection of methylene blue into the nucleus tractus solitarii [12].
• We report here that intravenously administered S-nitrosocysteine, a putative EDRF, and not the nitric oxide liberating compound sodium nitroprusside produces significant alterations in nociceptive behavior that are abolished by bilateral vagotomy [33].
• Immunohistochemistry study indicated that dehydration significantly increased the profiles of SON neurons co-expressing nitrosocysteine with BK-channel protein [6].

References