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Chemical Compound Review:

S-Nonap 2-acetamido-3-methyl-3- nitrososulfanyl...

Synonyms: snap, AG-G-56831, BSPBio_002446, KBioGR_001306, KBioSS_001933, ...

Müerköster, S. et al., Yasmin, W. et al., Ping, P. et al., Garbán, H.J. et al., Garg, U.C. et al., et al.

Romagnani, Lazzeri, Lasagni, Mavilia, Beltrame, Francalanci, Rotondi, Annunziato, Maurenzig, Cosmi, Galli, Salvadori, Maggi, Serio, Chang, Chan, Chan, Ping, Takano, Zhang, Tang, Qiu, Li, Banerjee, Dawn, Balafonova, Bolli, Terwel, Nieland, Schutte, Reutelingsperger, Ramaekers, Steinbusch, Rimmelzwaan, Baars, de Lijster, Fouchier, Osterhaus, Mei, Hord, Winterstein, Donald, Phang,

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Disease relevance of S-Nitroso-N-acetylpenicillamine

The role of NO. in the regulation of IRP1 and IRP2 in rat hepatoma cells was investigated by using the NO.-generating compound S-nitroso-N-acetylpenicillamine (SNAP), or by stimulating cells with multiple cytokines and lipopolysaccharide (LPS) to induce NO. production [1].
Similarly, upon treatment with S-nitroso-N-acetyl-DL-penicillamine (2-5 mM) or S-nitroso-glutathione (1-2 mM), human breast cancer cells (MCF-7), which express wild-type p53, rapidly accumulated p53 protein in the nuclei [2].
In the presence of the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP) (10(-8) mol/L topical suffusion), the dilation of pial arterioles (n = 5) to hypercapnia remained diminished (5 +/- 7%) at 2 hours after injury [3].
Another NO donor, S-nitroso-N-acetylpenicillamine (SNAP; 2.5 nmol), also produced immediate hypertension from 118+/-5 mm Hg to 168+/-7 mm Hg (P<.01) but without the second, long-lasting response [4].
Here we show that replication of influenza A and B viruses in Mabin Darby canine kidney cells is severely impaired by the NO donor, S-nitroso-N-acetylpenicillamine [5].

Psychiatry related information on S-Nitroso-N-acetylpenicillamine

This hypothesis was tested by microinjecting a control vehicle, NO donor, S-Nitroso-N-acetylpenicillamine (SNAP) and a competitive inhibitor of NO synthase enzyme (NOS), N(G)-Nitro-L-arginine methylester hydrochloride (L-NAME) into the PPT while quantifying the effects on wakefulness and sleep [6].
The possibility that NO is involved in the generation of motor activity in embryos of the frog Rana temporaria was investigated using the NO donors S-nitroso-n-acetylpenicillamine (SNAP; 100--500 micromol l(-1)) and diethylamine nitric oxide complex sodium (DEANO; 25--100 micromol l(-1)) [7].

High impact information on S-Nitroso-N-acetylpenicillamine

NO donors such as sodium nitroprusside and S-nitroso-N-acetyl-D,L-penicillamine markedly increase IL-1 beta-induced NO synthase mRNA and protein levels as well as enzyme activity [8].
Inhaling aerosol generated from S-nitroso-N-acetylpenicillamine also induced a rapid and profound decrease of RL from 0.453 +/- 0.022 to 0.287 +/- 0.022 cmH2O/ml.s, which lasted for over 15 min in guinea pigs broncho-constricted with methacholine [9].
The antimitogenic effect of S-nitroso-N-acetylpenicillamine was inhibited by hemoglobin and potentiated by superoxide dismutase, supporting the view that nitric oxide was the ultimate effector [10].
Sodium nitroprusside and S-nitroso-N-acetylpenicillamine significantly decreased the proliferation of vascular smooth muscle cells [10].
However, the relaxation in response to 8-bromo-cAMP, nitric oxide (NO), and the NO donor S-nitroso-N-acetylpenicillamine (SNAP), which circumvent plasma membrane receptors and directly activate intracellular mechanisms, was similar in gallbladders with cholesterol and pigment stones [11].

Chemical compound and disease context of S-Nitroso-N-acetylpenicillamine

Moreover, non-iron containing nitric oxide-donor compounds, such as S-nitroso-N-acetylpenicillamine, did not cause oxidative brain injury in vivo suggesting that nitric oxide may not mediate neurotoxicity induced by sodium nitroprusside [12].
In this work, we studied the effect of two NO donors, sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine SNP-treated on the response of wheat (Triticum aestivum) to water stress conditions [13].
Our objective was to measure the generation of ONOO- during reperfusion of isolated hearts subjected to ischemia and to determine the effects of inhibition of NO synthase with NG-monomethyl-L-arginine (L-NMMA), or supplementation of NO with S-nitroso-N-acetyl-D,L-penicillamine (SNAP), on ONOO- generation and on the recovery of mechanical function [14].
NO precursor, L-arginine and NO donors sodium nitroprusside, S-nitroso-N-acetylpenicillamine potentiated the hyperalgesia and allodynia significantly suggesting proalgesic effect in neuropathic rats [15].
By contrast, deferoxamine (iron chelator) attenuated the toxicity of sodium nitroprusside, but had no effect on the toxicity of S-nitroso-N-acetylpenicillamine [16].

Biological context of S-Nitroso-N-acetylpenicillamine

CHOP, a C/EBP homologous protein that is induced by endoplasmic reticulum (ER) stress and plays a role in growth arrest and cell death, was induced by a NO donor, S-nitroso-N-acetyl-D,L-penicillamine (SNAP) [17].
In the present study, we examined the effects of the NO donors sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) on cell cycle activity in VSMCs [18].
Incubation of T3M4 and PT45-P1 cells with the NO donor S-Nitroso-N-acetyl-D,L-penicillamine up-regulated IL-1beta secretion and conferred resistance toward etoposide-induced apoptosis [19].
Using the NO releasing agents S-nitroso-N-acetylpenicillamine and sodium nitroprusside it was determined that nitric oxide is sufficient to cause an increase in phosphorylation of p38 [20].
Using human monocytes as a model, we observed that nitrosothiol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine suppressed caspase-9 and caspase-3 activity and DNA fragmentation [21].

Anatomical context of S-Nitroso-N-acetylpenicillamine

Therefore, we tested the hypothesis that overexpression of MT reduces the sensitivity of NIH 3T3 cells to the .NO donor, S-nitrosoacetylpenicillamine (SNAP), and to .NO released from cells (NIH 3T3-DFG-iNOS) after infection with a retroviral vector expressing human iNOS gene [22].
This report demonstrates that authentic NO.and the NO.-generating compound S-nitroso-N-acetylpenicillamine inhibit hepatocyte total protein synthesis in a reversible and concentration-dependent fashion [23].
Three such agents, S-nitroso-N-acetylpenicillamine (SNAP), diethylenetriamine NO adduct (DETA-NO), and sodium nitroprusside provide (SNP), were found to promote complete short-term survival after removal of serum from naive PC12 cells and of NGF from neuronally differentiated PC12 cells and sympathetic neurons [24].
Cultured bovine aortic endothelial cells exposed to the NO donors sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) resulted in increased heme oxygenase activity and HO-1 expression [25].
To elucidate the mechanism underlying this process, we investigated the effect of S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide-releasing agent, on the smooth muscle cell cycle [26].

Associations of S-Nitroso-N-acetylpenicillamine with other chemical compounds

Conversely, a translocation of PKCepsilon and -eta quantitatively similar to that induced by ischemic PC could be reproduced pharmacologically with the administration of 2 structurally unrelated NO donors, diethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at doses previously shown to elicit a late PC effect [27].
NO donors such as S-nitroso-n-acetylpenicillamine and S-nitrosoglutathione (both at 0.01-100 microM) inhibited TCIPA and MMP-2 release from platelets and tumor cells [28].
Since S-nitroso-N-acetylpenicillamine did not increase either cGMP or cAMP, NO did not increase cGMP, and 8-bromo-cGMP did not alter cytosolic free calcium, we conclude that NO decreases cytosolic free calcium by a cyclic nucleotide-independent mechanism in Balb/c 3T3 fibroblasts [29].
Transient transfection of AD10 cells with pGL-3-FasP demonstrated that the IFN-gamma-dependent NO generation increases the trans-activation of the Fas promoter, and this increase was blocked by the NOS inhibitor (N(G)-monomethyl-L-arginine), but could be restored by the addition of the NO donor S-nitroso-N-acetylpenicillamine [30].
The NO donor S-nitroso-N-acetylpenicillamine, adenoviral transfer of inducible NO synthase gene, and antioxidants (alpha-tocopherol and superoxide dismutase plus catalase) but not oxidized SNAP, 8-Br-cGMP, nitrite, and nitrate, suppressed ROS production, p53-dependent Noxa expression, and apoptosis induced by HCy [31].

Gene context of S-Nitroso-N-acetylpenicillamine

Using electrophoretic mobility shift assays, we found that NO-releasing agents (E)-methyl-2-[(E)-hydroxyimino]-5-nitro-6-methoxy-3-hexeneamide and S-nitroso-N-acetylpenicillamine greatly enhanced the formation of beta-catenin/LEF-1 DNA binding complex in a concentration- and time-dependent fashion in YAMC and IMCE cells [32].
When FLS were cultured with S-nitroso-N-acetylpenicillamine, the pattern of MMR expression in RA synovium was reproduced (high hMSH3, low hMSH6) [33].
The NO donor S-nitroso-N-acetyl-DL-penicillamine inhibited caspase-1 activity in cells as well as the activity of purified recombinant caspase-1 and also prevented the cleavage of pro-IL-1beta and pro-IGIF by recombinant caspase-1 [34].
The induction of IP-10 and Mig mRNA and protein expression by IFN-gamma plus TNF-alpha was strongly inhibited by nitric oxide (NO) donors, such as sodium nitroprusside or S-nitroso-N-acetylpenicillamine, but not by cGMP analogues [35].
The induction of p21 by the NO donor S-nitroso-N-acetylpenicillamine (SNAP) seemed to be due to transactivation because SNAP elevated the activity of p21 promoter but did not stabilize p21 mRNA and protein [36].

Analytical, diagnostic and therapeutic context of S-Nitroso-N-acetylpenicillamine

Using the in situ perfusion of normal and cirrhotic rat livers, we compared the vascular relaxation induced by either NTG or the spontaneous nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) [37].
An NO donor, S-nitroso-N-acetylpenicillamine (SNAP), suppressed apoptosis of NK cells induced by CD16 cross-linking or coculture with target cells, suggesting that endogenous NO production is involved in protection of NK cells from activation-induced apoptosis, thereby maintaining NK activity [38].
METHODS: We tested for modulatory effects of the nitric oxide (NO) donors S-nitroso-N-acetyl-D,L-penicillamine and DETA-NONOate, and the superoxide-generating system hypoxanthine/xanthine oxidase (HXXO) on the expression and activity of tissue plasminogen activator (tPA) by ELISA and Northern blotting [39].
Western blot analysis demonstrated that rFasL significantly up-regulated caspase-3, -8, and -9 activities in granulosa cells, which were attenuated by concurrent treatment with S-nitroso-N-acetylpenicillamine [40].
Microinjection bilaterally of a NO donor, S-nitroso-N-acetylpenicillamine (0.25 or 1 nmoles), or the NO precursor, L-arginine (1 or 5 nmoles), into the hippocampal CA1 or CA3 subfield or dentate gyrus elicited a significant reduction in baseline ICP [41].

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