Nitroso compounds are organic or inorganic substances containing the nitroso functional group, which consists of a nitrogen atom bonded to an oxygen atom through a single covalent bond, often abbreviated as -NO.
A macrolide antibiotic produced by Streptomyces kitasatoensis. The drug has antimicrobial activity against a wide spectrum of pathogens.
A bacteriostatic antibacterial agent that interferes with folic acid synthesis in susceptible bacteria. Its broad spectrum of activity has been limited by the development of resistance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p208)
Conversion into nitroso compounds. An example is the reaction of nitrites with amino compounds to form carcinogenic N-nitrosamines.
Inorganic oxides that contain nitrogen.
Diethylamines are organic compounds consisting of two ethyl groups bonded to an amino nitrogen atom, with the general formula (C2H5)2NH, known for their foul odor and use as chemical intermediates in various industrial applications, but notably not associated with medical definitions unless referring to potential substance abuse or intoxication.
Changing an open-chain hydrocarbon to a closed ring. (McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
A class of compounds that contain a -NH2 and a -NO radical. Many members of this group have carcinogenic and mutagenic properties.
Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)
Compounds containing the -SH radical.
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.
The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
The rate dynamics in chemical or physical systems.

Inhibition of transforming growth factor beta production by nitric oxide-treated chondrocytes: implications for matrix synthesis. (1/487)

OBJECTIVE: Nitric oxide (NO) is generated copiously by articular chondrocytes activated by interleukin-1beta (IL-1beta). If NO production is blocked, much of the IL-1beta inhibition of proteoglycan synthesis is prevented. We tested the hypothesis that this inhibitory effect of NO on proteoglycan synthesis is secondary to changes in chondrocyte transforming growth factor beta (TGFbeta). METHODS: Monolayer, primary cultures of lapine articular chondrocytes and cartilage slices were studied. NO production was determined as nitrite accumulation in the medium. TGFbeta bioactivity in chondrocyte- and cartilage-conditioned medium (CM) was measured with the mink lung epithelial cell bioassay. Proteoglycan synthesis was measured as the incorporation of 35S-sodium sulfate into macromolecules separated from unincorporated label by gel filtration on PD-10 columns. RESULTS: IL-1beta increased active TGFbeta in chondrocyte CM by 12 hours; by 24 hours, significant increases in both active and latent TGFbeta were detectable. NG-monomethyl-L-arginine (L-NMA) potentiated the increase in total TGFbeta without affecting the early TGFbeta activation. IL-1beta stimulated a NO-independent, transient increase in TGFbeta3 at 24 hours; however, TGFbeta1 was not changed. When NO synthesis was inhibited with L-NMA, IL-1beta increased CM concentrations of TGFbeta1 from 24-72 hours of culture. L-arginine (10 mM) reversed the inhibitory effect of L-NMA on NO production and blocked the increases in TGFbeta1. Anti-TGFbeta1 antibody prevented the restoration of proteoglycan synthesis by chondrocytes exposed to IL-1beta + L-NMA, confirming that NO inhibition of TGFbeta1 in IL-1beta-treated chondrocytes effected, in part, the decreased proteoglycan synthesis. Furthermore, the increase in TGFbeta and proteoglycan synthesis seen with L-NMA was reversed by the NO donor S-nitroso-N-acetylpenicillamide. Similar results were seen with cartilage slices in organ culture. The autocrine increase in CM TGFbeta1 levels following prior exposure to TGFbeta1 was also blocked by NO. CONCLUSION: NO can modulate proteoglycan synthesis indirectly by decreasing the production of TGFbeta1 by chondrocytes exposed to IL-1beta. It prevents autocrine-stimulated increases in TGFbeta1, thus potentially diminishing the anabolic effects of this cytokine in chondrocytes.  (+info)

In vitro simultaneous measurements of relaxation and nitric oxide concentration in rat superior mesenteric artery. (2/487)

1. The relationship between nitric oxide (NO) concentration measured with an NO-specific microelectrode and endothelium-dependent relaxation was investigated in isolated rat superior mesenteric artery contracted with 1 microM noradrenaline. 2. Acetylcholine (10 microM) induced endothelium-dependent simultaneous increases in luminal NO concentration of 21 +/- 6 nM, and relaxations with pD2 values and maximum of 6.95 +/- 0.32 and 97.5 +/- 0.7 % (n = 7), respectively. An inhibitor of NO synthase, N G-nitro-L-arginine (L-NOARG, 100 microM) inhibited the relaxations and increases in NO concentration induced by acetylcholine. 3. Oxyhaemoglobin (10 microM) reversed the relaxations and increases in NO concentrations induced by acetylcholine, S-nitroso-N-acetylpenicillamine (SNAP) and S-morpholino-sydnonimine (SIN-1), but not the relaxations induced with forskolin. Oxyhaemoglobin also decreased the NO concentration below baseline level. 4. In the presence of L-NOARG (100 microM), a small relaxation to acetylcholine (10 microM) of noradrenaline-contracted segments was still seen; oxyhaemogobin inhibited this relaxation and decreased the NO concentration by 14 +/- 4 nM (n = 4). 5. The NO concentration-relaxation relationship for acetylcholine resembled that for SNAP and SIN-1 more than for authentic NO. Thus while 7-17 nM NO induced half-maximal relaxations in response to SNAP or SIN-1, 378 +/- 129 nM NO (n = 4) was needed for half-maximal relaxation to authentic NO. 6. The present study provides direct evidence that the relaxation of the rat superior mesenteric artery with the endothelium-dependent vasodilator acetylcholine is correlated to the endogeneous release of NO. The study also suggests that NO mediates the L-NOARG-resistant relaxations in this artery, and that there is a basal NO release.  (+info)

S-nitrosoglutathione enhances neutrophil DNA fragmentation and cell death. (3/487)

Enhancing the clearance of neutrophils by enhancing apoptotic cell death and macrophage recognition may be beneficial in acute lung injury. Exogenous nitric oxide gas depresses neutrophil oxidative functions and accelerates cell death (A. H. Daher, J. D. Fortenberry, M. L. Owens, and L. A. Brown. Am. J. Respir. Cell Mol. Biol. 16: 407-412, 1997). We hypothesized that S-nitrosoglutathione (GSNO), a physiologically relevant nitric oxide donor, could also enhance neutrophil DNA fragmentation. Neutrophils were incubated for 2-24 h in the absence and presence of GSNO (dose range 0.1-5 mM) and evaluated for cell death by a fluorescent viability/cytotoxicity assay. Neutrophil DNA fragmentation was assessed by cell death detection ELISA and by terminal deoxynucleotidyltransferase-mediated fluorescence-labeled dUTP nick end labeling assay. Neutrophil oxidative function was also determined. Incubation with GSNO increased cell death at 2, 4, and 24 h. GSNO incubation for 24 h significantly increased DNA fragmentation in a dose-dependent fashion at 0.5 (median 126% of control value; P = 0.002) and 5 mM (185% of control value; P = 0.002) by terminal deoxynucleotidyltransferase-mediated fluorescence-labeled dUTP nick end labeling and at 0.5 mM by ELISA (164% of control value; P = 0.03). The apoptosis-to-total cell death ratio increased with increasing GSNO concentration (P < 0.05). Effects were mitigated by coincubation with superoxide dismutase. Five millimolar GSNO decreased overall superoxide generation and O2 consumption but not when adjusted for dead neutrophils. GSNO significantly enhances cell death and neutrophil DNA fragmentation in a dose-dependent fashion.  (+info)

Tonic and phasic influences of nitric oxide on renal blood flow autoregulation in conscious dogs. (4/487)

The aim of this study was to investigate the influence of the mean level and phasic modulation of NO on the dynamic autoregulation of renal blood flow (RBF). Transfer functions were calculated from spontaneous fluctuations of RBF and arterial pressure (AP) in conscious resting dogs for 2 h under control conditions, after NO synthase (NOS) inhibition [NG-nitro-L-arginine methyl ester hydrochloride (L-NAME)] and after L-NAME followed by a continuous infusion of an NO donor [S-nitroso-N-acetyl-DL-penicillamine (SNAP)]. After L-NAME (n = 7) AP was elevated, heart rate (HR) and RBF were reduced. The gain of the transfer function above 0.08 Hz was increased, compatible with enhanced resonance of the myogenic response. A peak of high gain around 0.03 Hz, reflecting oscillations of the tubuloglomerular feedback (TGF), was not affected. The gain below 0.01 Hz, was elevated, but still less than 0 dB, indicating diminished but not abolished autoregulation. After L-NAME and SNAP (n = 5), mean AP and RBF were not changed, but HR was slightly elevated. The gain above 0.08 Hz and the peak of high gain at 0.03 Hz were not affected. The gain below 0.01 Hz was elevated, but smaller than 0 dB. It is concluded that NO may help to prevent resonance of the myogenic response depending on the mean level of NO. The feedback oscillations of the TGF are not affected by NO. NO contributes to the autoregulation below 0.01 Hz due to phasic modulation independent of its mean level.  (+info)

Ovarian hormone secretory response to gonadotropins and nitric oxide following chronic nitric oxide deficiency in the rat. (5/487)

Ovarian hormone secretion is regulated by gonadotropins, and it has been demonstrated that this response is modulated by nitric oxide (NO). The focus of this study was to determine the effect of chronic NO deficiency on the secretion of ovarian steroids. Female rats were given N-nitro-L-arginine (L-NNA; 0.6 g/L) in their drinking water, and vaginal smears were obtained daily. By 4 wk of treatment, all the rats were in constant estrus or proestrus. At 6-8 wk the animals were killed; the ovaries were removed and incubated in the presence of eCG (1 IU/ml) and hCG (1 IU/ml) and/or S-nitroso-L-acetyl penicillamine (an NO donor, S-NAP; 0.1 mM) for 4 h. Medium was collected at 30-min intervals, and estradiol, progesterone, and androstenedione were measured. Ovaries from proestrous rats served as controls. Ovaries from L-NNA-treated animals had a greater basal and gonadotropin-stimulated release of estradiol but not of androstenedione or progesterone in comparison to ovaries from untreated controls. S-NAP decreased the gonadotropin-stimulated estradiol, progesterone, and androstenedione in ovaries from NO-deficient rats. Steroid secretion in controls was not responsive to S-NAP. We conclude that chronic NO inhibition produces constant estrus due to increased estradiol production and that NO acts to inhibit estradiol and androstenedione production.  (+info)

Stimulation of cystine uptake by nitric oxide: regulation of endothelial cell glutathione levels. (6/487)

Nitric oxide (NO) is known to produce some of its biological activity through modification of cellular thiols. Return of cellular thiols to their basal state requires the activity of the GSH redox cycle, suggesting important interactions between NO signaling and regulation of cellular redox status. Because continuous exposure to NO may lead to adaptive responses in cellular redox systems, we investigated the effects of NO on cellular GSH levels in vascular endothelial cells. Acute exposure (1 h) of cells to >1 mM S-nitroso-N-acetyl-penicillamine (SNAP) led to depletion of GSH. On the other hand, chronic exposure to lower concentrations of SNAP (+info)

Regulation of intracellular polyamine biosynthesis and transport by NO and cytokines TNF-alpha and IFN-gamma. (7/487)

Nitric oxide (NO) has been described to exert cytostatic effects on cellular proliferation; however the mechanisms responsible for these effects have yet to be fully resolved. Polyamines, conversely, are required components of cellular proliferation. In experimental models of inflammation, a relationship between these two pathways has been suggested by the temporal regulation of a common precursor, arginine. This study was undertaken to determine the effects NO and the NO synthase (NOS)-inducing cytokines, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), exert on polyamine regulation. The transformed kidney proximal tubule cell line, MCT, maintains high constitutive levels of the first polyamine biosynthetic enzyme, ornithine decarboxylase (ODC). NO donors markedly suppressed ODC activity in MCT and all other cell lines examined. TNF-alpha and IFN-gamma induction of NO generation resulted in suppressed ODC activity, an effect prevented by the inducible NOS inhibitor L-N6-(1-iminoethyl)lysine (L-NIL). Dithiothreitol reversal of NO-mediated ODC suppression supports nitrosylation as the mechanism of inactivation. We also evaluated polyamine uptake, inasmuch as inhibition of ODC can result in a compensatory induction of polyamine transporters. Administration of NO donors, or TNF-alpha and IFN-gamma, suppressed [3H]putrescine uptake, thereby preventing transport-mediated reestablishment of intracellular polyamine levels. This study demonstrates the capacity of NO and inflammatory cytokines to regulate both polyamine biosynthesis and transport.  (+info)

Glyceryl trinitrate-induced vasodilation is inhibited by ultraviolet irradiation despite enhanced nitric oxide generation: evidence for formation of a nitric oxide conjugate. (8/487)

Our objective was to determine whether a stabilized form of nitric oxide (NO) such as an S-nitrosothiol, rather than NO itself, is the vasoactive metabolite produced when glyceryl trinitrate (GTN) interacts with vascular smooth muscle. In a control study, NO formation was measured by a chemiluminescence-headspace gas method during the incubation of a prototype S-nitrosothiol, namely, S-nitroso-N-acetylpenicillamine (SNAP), in Krebs' solution. NO formation from SNAP was increased when the incubation was carried out in the presence of UV light, indicating that homolytic photolysis of the S-nitrosothiol had occurred. When GTN was incubated with bovine pulmonary artery (BPA) in the absence of UV light, NO was not measurable until 5 min of incubation. By contrast, in the presence of UV light, NO was measurable as early as 0.5 min, and by 5 min, it was higher than that observed in the absence of UV light. BPA rings were relaxed with SNAP and GTN in the absence of UV light, and EC50 values of 0.24 +/- 0.28 microM and 10 +/- 6 nM, respectively, were observed. In the presence of UV light, the vasodilator response of BPA to SNAP and GTN was attenuated, and EC50 values of 2.7 +/- 3.0 microM and 49 +/- 23 nM, respectively, were observed. Our results are consistent with the idea that GTN biotransformation by vascular smooth muscle results in the production of a stabilized form of NO, possibly an S-nitrosothiol, and that degradation of this metabolite by UV light results in NO formation accompanied by decreased vasodilation.  (+info)

Nitroso compounds are a class of chemical compounds that contain a nitroso functional group, which is composed of a nitrogen atom bonded to an oxygen atom with a single covalent bond. The general formula for nitroso compounds is R-N=O, where R represents an organic group such as an alkyl or aryl group.

Nitroso compounds are known to be reactive and can form under various physiological conditions. They have been implicated in the formation of carcinogenic substances and have been linked to DNA damage and mutations. In the medical field, nitroso compounds have been studied for their potential use as therapeutic agents, particularly in the treatment of cancer and cardiovascular diseases. However, their use is limited due to their potential toxicity and carcinogenicity.

It's worth noting that exposure to high levels of nitroso compounds can be harmful to human health, and may cause respiratory, dermal, and ocular irritation, as well as potential genotoxic effects. Therefore, handling and storage of nitroso compounds should be done with caution, following appropriate safety guidelines.

Kitasamycin is an antibiotic that belongs to the class of drugs known as macrolides. It is derived from the bacterium Streptomyces murayamaensis and is primarily used in veterinary medicine for the treatment of various bacterial infections in animals. The mechanism of action of kitasamycin involves inhibiting protein synthesis in bacteria by binding to their ribosomes.

In human medicine, kitasamycin has been investigated as a potential therapeutic option for certain types of bacterial infections, such as those caused by Mycobacterium avium complex (MAC) in patients with HIV/AIDS. However, its use in humans is not widely approved and remains limited to clinical trials and investigational settings.

It's important to note that the use of antibiotics, including kitasamycin, should be reserved for treating bacterial infections and should not be used indiscriminately or without proper medical supervision, as misuse can contribute to antibiotic resistance.

Sulfamethoxazole is a type of antibiotic known as a sulfonamide. It works by interfering with the ability of bacteria to produce folic acid, which is necessary for their growth and survival. Sulfamethoxazole is often combined with trimethoprim (another antibiotic) in a single medication called co-trimoxazole, which is used to treat a variety of bacterial infections, including respiratory tract infections, urinary tract infections, and skin and soft tissue infections.

The medical definition of Sulfamethoxazole can be found in various pharmaceutical and medical resources, here are some examples:

* According to the Merck Manual, Sulfamethoxazole is a "synthetic antibacterial drug that inhibits bacterial synthesis of folic acid by competing with para-aminobenzoic acid for the enzyme dihydropteroate synthetase."
* According to the British National Formulary (BNF), Sulfamethoxazole is a "sulfonamide antibacterial agent, active against many Gram-positive and Gram-negative bacteria. It is often combined with trimethoprim in a 5:1 ratio as co-trimoxazole."
* According to the National Library of Medicine (NLM), Sulfamethoxazole is a "synthetic antibacterial agent that is used in combination with trimethoprim for the treatment of various bacterial infections. It works by inhibiting the bacterial synthesis of folic acid."

It's important to note that, as any other medication, Sulfamethoxazole should be taken under medical supervision and following the instructions of a healthcare professional, as it can cause side effects and interact with other medications.

Nitrosation is a chemical reaction that involves the addition of a nitrosonium ion (NO+) to another molecule. In the context of medicine, particularly in relation to gastroenterology and oncology, nitrosation is often discussed in terms of its potential role in the formation of carcinogenic N-nitroso compounds (NOCs).

These NOCs can be formed when nitrites (compounds containing a nitrite ion, NO2-) or nitrous acid (HNO2) react with secondary amines or other amino compounds under acidic conditions. This reaction can occur in the stomach after the ingestion of foods or beverages that contain both nitrites and amines, such as processed meats and certain alcoholic beverages.

The formation of NOCs has been associated with an increased risk of various types of cancer, including gastric and esophageal cancer. However, it's important to note that the relationship between nitrosation and cancer is complex and not fully understood, as other factors such as the presence of antioxidants in the diet can also influence the formation of NOCs.

Nitrogen oxides (NOx) are a group of highly reactive gases, primarily composed of nitric oxide (NO) and nitrogen dioxide (NO2). They are formed during the combustion of fossil fuels, such as coal, oil, gas, or biomass, and are emitted from various sources, including power plants, industrial boilers, transportation vehicles, and residential heating systems. Exposure to NOx can have adverse health effects, particularly on the respiratory system, and contribute to the formation of harmful air pollutants like ground-level ozone and fine particulate matter.

Diethylamines are organic compounds that consist of a nitrogen atom bonded to two ethyl groups and one hydrogen atom. The chemical formula for diethylamine is (C2H5)2NH, and it is a colorless liquid with an unpleasant fishy odor. It is used as a building block in the synthesis of various pharmaceuticals, agrochemicals, and other organic compounds. Diethylamines can also be found as byproducts in some industrial processes and are produced naturally by certain plants and animals.

Diethylamines can have stimulant effects on the central nervous system and can cause symptoms such as excitement, restlessness, and confusion. In high concentrations or with prolonged exposure, diethylamines can be toxic and may cause respiratory, cardiovascular, and neurological problems. Therefore, it is important to handle diethylamines with care and use appropriate safety measures when working with them.

Cyclization is a chemical process that involves forming a cyclic structure or ring-shaped molecule from a linear or open-chain compound. In the context of medicinal chemistry and drug design, cyclization reactions are often used to synthesize complex molecules, including drugs, by creating rings or fused ring systems within the molecule's structure.

Cyclization can occur through various mechanisms, such as intramolecular nucleophilic substitution, electrophilic addition, or radical reactions. The resulting cyclized compounds may exhibit different chemical and biological properties compared to their linear precursors, making them valuable targets for drug discovery and development.

In some cases, the cyclization process can lead to the formation of stereocenters within the molecule, which can impact its three-dimensional shape and how it interacts with biological targets. Therefore, controlling the stereochemistry during cyclization reactions is crucial in medicinal chemistry to optimize the desired biological activity.

Overall, cyclization plays a significant role in the design and synthesis of many pharmaceutical compounds, enabling the creation of complex structures that can interact specifically with biological targets for therapeutic purposes.

Nitrosamines are a type of chemical compound that are formed by the reaction between nitrous acid (or any nitrogen oxide) and secondary amines. They are often found in certain types of food, such as cured meats and cheeses, as well as in tobacco products and cosmetics.

Nitrosamines have been classified as probable human carcinogens by the International Agency for Research on Cancer (IARC). Exposure to high levels of nitrosamines has been linked to an increased risk of cancer, particularly in the digestive tract. They can also cause DNA damage and interfere with the normal functioning of cells.

In the medical field, nitrosamines have been a topic of concern due to their potential presence as contaminants in certain medications. For example, some drugs that contain nitrofurantoin, a medication used to treat urinary tract infections, have been found to contain low levels of nitrosamines. While the risk associated with these low levels is not well understood, efforts are underway to minimize the presence of nitrosamines in medications and other products.

In a medical context, nitrites are typically referred to as organic compounds that contain a functional group with the formula R-N=O, where R represents an alkyl or aryl group. They are commonly used in medicine as vasodilators, which means they widen and relax blood vessels, improving blood flow and lowering blood pressure.

One example of a nitrite used medically is amyl nitrite, which was previously used to treat angina pectoris, a type of chest pain caused by reduced blood flow to the heart muscle. However, its use has largely been replaced by other medications due to safety concerns and the availability of more effective treatments.

It's worth noting that inorganic nitrites, such as sodium nitrite, are also used in medicine for various purposes, including as a preservative in food and as a medication to treat cyanide poisoning. However, these compounds have different chemical properties and uses than organic nitrites.

Sulfhydryl compounds, also known as thiol compounds, are organic compounds that contain a functional group consisting of a sulfur atom bonded to a hydrogen atom (-SH). This functional group is also called a sulfhydryl group. Sulfhydryl compounds can be found in various biological systems and play important roles in maintaining the structure and function of proteins, enzymes, and other biomolecules. They can also act as antioxidants and help protect cells from damage caused by reactive oxygen species. Examples of sulfhydryl compounds include cysteine, glutathione, and coenzyme A.

Drug hypersensitivity is an abnormal immune response to a medication or its metabolites. It is a type of adverse drug reaction that occurs in susceptible individuals, characterized by the activation of the immune system leading to inflammation and tissue damage. This reaction can range from mild symptoms such as skin rashes, hives, and itching to more severe reactions like anaphylaxis, which can be life-threatening.

Drug hypersensitivity reactions can be classified into two main types: immediate (or IgE-mediated) and delayed (or non-IgE-mediated). Immediate reactions occur within minutes to a few hours after taking the medication and are mediated by the release of histamine and other inflammatory mediators from mast cells and basophils. Delayed reactions, on the other hand, can take several days to develop and are caused by T-cell activation and subsequent cytokine release.

Common drugs that can cause hypersensitivity reactions include antibiotics (such as penicillins and sulfonamides), nonsteroidal anti-inflammatory drugs (NSAIDs), monoclonal antibodies, and chemotherapeutic agents. It is important to note that previous exposure to a medication does not always guarantee the development of hypersensitivity reactions, as they can also occur after the first administration in some cases.

The diagnosis of drug hypersensitivity involves a thorough medical history, physical examination, and sometimes skin or laboratory tests. Treatment typically includes avoiding the offending medication and managing symptoms with antihistamines, corticosteroids, or other medications as needed. In severe cases, emergency medical care may be required to treat anaphylaxis or other life-threatening reactions.

Molecular structure, in the context of biochemistry and molecular biology, refers to the arrangement and organization of atoms and chemical bonds within a molecule. It describes the three-dimensional layout of the constituent elements, including their spatial relationships, bond lengths, and angles. Understanding molecular structure is crucial for elucidating the functions and reactivities of biological macromolecules such as proteins, nucleic acids, lipids, and carbohydrates. Various experimental techniques, like X-ray crystallography, nuclear magnetic resonance (NMR) spectroscopy, and cryo-electron microscopy (cryo-EM), are employed to determine molecular structures at atomic resolution, providing valuable insights into their biological roles and potential therapeutic targets.

Stereoisomerism is a type of isomerism (structural arrangement of atoms) in which molecules have the same molecular formula and sequence of bonded atoms, but differ in the three-dimensional orientation of their atoms in space. This occurs when the molecule contains asymmetric carbon atoms or other rigid structures that prevent free rotation, leading to distinct spatial arrangements of groups of atoms around a central point. Stereoisomers can have different chemical and physical properties, such as optical activity, boiling points, and reactivities, due to differences in their shape and the way they interact with other molecules.

There are two main types of stereoisomerism: enantiomers (mirror-image isomers) and diastereomers (non-mirror-image isomers). Enantiomers are pairs of stereoisomers that are mirror images of each other, but cannot be superimposed on one another. Diastereomers, on the other hand, are non-mirror-image stereoisomers that have different physical and chemical properties.

Stereoisomerism is an important concept in chemistry and biology, as it can affect the biological activity of molecules, such as drugs and natural products. For example, some enantiomers of a drug may be active, while others are inactive or even toxic. Therefore, understanding stereoisomerism is crucial for designing and synthesizing effective and safe drugs.

Oxidation-Reduction (redox) reactions are a type of chemical reaction involving a transfer of electrons between two species. The substance that loses electrons in the reaction is oxidized, and the substance that gains electrons is reduced. Oxidation and reduction always occur together in a redox reaction, hence the term "oxidation-reduction."

In biological systems, redox reactions play a crucial role in many cellular processes, including energy production, metabolism, and signaling. The transfer of electrons in these reactions is often facilitated by specialized molecules called electron carriers, such as nicotinamide adenine dinucleotide (NAD+/NADH) and flavin adenine dinucleotide (FAD/FADH2).

The oxidation state of an element in a compound is a measure of the number of electrons that have been gained or lost relative to its neutral state. In redox reactions, the oxidation state of one or more elements changes as they gain or lose electrons. The substance that is oxidized has a higher oxidation state, while the substance that is reduced has a lower oxidation state.

Overall, oxidation-reduction reactions are fundamental to the functioning of living organisms and are involved in many important biological processes.

Nitric oxide (NO) is a molecule made up of one nitrogen atom and one oxygen atom. In the body, it is a crucial signaling molecule involved in various physiological processes such as vasodilation, immune response, neurotransmission, and inhibition of platelet aggregation. It is produced naturally by the enzyme nitric oxide synthase (NOS) from the amino acid L-arginine. Inhaled nitric oxide is used medically to treat pulmonary hypertension in newborns and adults, as it helps to relax and widen blood vessels, improving oxygenation and blood flow.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

... (SNAP) is the organosulfur compound with the formula ONSC(CH3)2CH(NHAc)CO2H. It is a green ... "N3398 h S-Nitroso-N-acetyl-DL-penicillamine". Sigma-Aldric. Retrieved 13 December 2021. Arulsamy, N.; Bohle, D. S.; Butt, J. A ... class of S-nitrosothiols which have received much attention in biochemistry because nitric oxide and some organic nitroso ...
S-Nitrosoglutathione (GSNO) S-Nitroso-N-acetylpenicillamine (SNAP) S-Nitrosotriphenylmethanethiol "Nitroso" IUPAC nomenclature ... The addition of a nitroso group to a sulfur atom of an amino acid residue of a protein is known as S-nitrosylation or S- ... Articles with short description, Short description is different from Wikidata, Functional groups, Nitroso compounds, Sulfur ... are organic compounds or functional groups containing a nitroso group attached to the sulfur atom of a thiol. S-Nitrosothiols ...
Park YK, Ahn DR, Oh M, Lee T, Yang EG, Son M, Park H (July 2008). "Nitric oxide donor, (+/-)-S-nitroso-N-acetylpenicillamine, ...
Park YK, Ahn DR, Oh M, Lee T, Yang EG, Son M, Park H (July 2008). "Nitric oxide donor, (+/-)-S-nitroso-N-acetylpenicillamine, ...
Park YK, Ahn DR, Oh M, Lee T, Yang EG, Son M, Park H (July 2008). "Nitric oxide donor, (+/-)-S-nitroso-N-acetylpenicillamine, ...
... s-nitroso-n-acetylpenicillamine MeSH D12.125.166.800 - thiopronine MeSH D12.125.166.893 - thiorphan MeSH D12.125.190.055 - ...
... s-nitroso-n-acetylpenicillamine MeSH D02.886.489.725.750 - s-nitrosoglutathione MeSH D02.886.489.750 - succimer MeSH D02.886. ... s-nitroso-n-acetylpenicillamine MeSH D02.654.846.500.249 - s-nitrosoglutathione MeSH D02.675.276.046 - ambenonium chloride MeSH ... s-nitroso-n-acetylpenicillamine MeSH D02.886.030.800 - thiopronine MeSH D02.886.030.893 - thiorphan MeSH D02.886.092.408 - ...
... the fourth derivative of the position vector with respect to time S-Nitroso-N-acetylpenicillamine, a chemical compound Schedule ...
  • S-Nitroso-N-acetylpenicillamine (SNAP) is the organosulfur compound with the formula ONSC(CH3)2CH(NHAc)CO2H. (wikipedia.org)
  • SNAP is an S-nitrosothiol and is used as a model for the general class of S-nitrosothiols which have received much attention in biochemistry because nitric oxide and some organic nitroso derivatives serve as signaling molecules in living systems, especially related to vasodilation. (wikipedia.org)
  • In this study, Tygon® PVC tubing was impregnated with a NO donor molecule, S-nitroso-N-acetylpenicillamine (SNAP), via a simple solvent-swelling-impregnation method, where polymer samples were submerged in a SNAP impregnation-solvent (methanol, acetone, plasticizer). (ucf.edu)
  • Cell viability in simulated ischemia/reperfusion (SI/R)-induced injury and a known cardiocytoprotective NO-donor, S-nitroso-n-acetylpenicillamine (SNAP) was tested. (nih.gov)
  • They treated the cells with a chemical called SNAP (S-nitroso-N-acetylpenicillamine), which generates nitric oxide. (medicalnewstoday.com)
  • S -Nitroso- N -acetylpenicillamine (SNAP), sodium nitroprusside (SNP), and S -nitrosoglutathione (GSNO). (kennesaw.edu)
  • LTD is also induced by the NO donors S-nitroso-N-acetylpenicillamine (SNAP) and hydroxylamine. (torvergata.it)
  • We examined the effect of an NO producer, S-nitroso-acetyl-penicillamine (SNAP), on the growth and survival in vitro of P. chabaudi AS, P. berghei and P. falciparum. (ncl.ac.uk)
  • In this paper, we, for the first time, demonstrate that the concentration of buffer remarkably affects the stability of RSNOs including naturally occurring S-nitrosoglutathione (GSNO) and synthetic S-nitroso-N-acetylpenicillamine (SNAP). (allergy-link.com)
  • To establish if NO leads to biochemical and cellular ASD-like phenotypes, C57BL/6J wild-type (WT) male mice were treated with an NO donor, S-nitroso-N-acetyl penicillamine (SNAP). (beyondair.net)
  • Treatment of cells with S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, was shown to induce cell death, and treatment with melatonin (100 μm) significantly attenuated the occurrence of NO-induced cell death. (elsevierpure.com)
  • Conversely, bolus injections of authentic NO or S-nitroso-N-acetyl penicillamine accelerate repriming in intact vessels and restore photorelaxation in endothelium-deficient preparations. (uhi.ac.uk)
  • 17. Nitric oxide donor, (+/-)-S-nitroso-N-acetylpenicillamine, stabilizes transactive hypoxia-inducible factor-1alpha by inhibiting von Hippel-Lindau recruitment and asparagine hydroxylation. (nih.gov)
  • An organic NO donor, S-nitroso-N-acetylpenicillamine, significantly inhibited the replication cycle of SARS CoV in a concentration-dependent manner. (nitricoxideinnovations.com)
  • An NO-independent IL-1 signalling pathway facilitates CYP2B proteins down-regulation by an NO donor We shown previously the 4-Demethylepipodophyllotoxin manufacture NO donor substances NOC-18, em S /em -nitroso- em N /em -acetylpenicillamine and em S /em -nitrosoglutath-ione could all down-regulate CYP2B protein in rat hepatocytes [26], which NOC-18 may possibly also down-regulate CYP2B6?in human being hepatocytes [27]. (gasyblog.com)
  • In scramble MIN6 cells or wild-type islets, acute exposure to oxidative stressors, including hydrogen peroxide (H 2 O 2 ) and S-nitroso-N-acetylpenicillamine, resulted in cell damage as determined by decrease in cell viability, reduced ATP content, morphology changes of islets, and/or alterations of apoptotic biomarkers in a concentration- and/or time-dependent manner. (hindawi.com)
  • This effect was NO-dependent, and treatment of cells with the NO donors (Z)-1-[2-(2-aminoethyl)-N-(2-ammonioethyl) aminodiazen-1-ium-1,2-diolate (NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamine also suppressed CYP2B proteins. (nih.gov)
  • With real-time confocal microscopy, the effect of three nitric oxide (NO) donors, S-nitroso-N-acetylpenicillamine, S-nitrosoglutathione, and diethylamine NO adduct, on the dynamic intracellular Ca 2+ concentration ([Ca 2+ ](i)) response of porcine tracheal smooth muscle (TSM) cells to acetylcholine (ACh) was examined. (elsevierpure.com)
  • The nitric oxide-releasing agent S-nitro-N-acetylpenicillamine and 2,2-diethyl-1-nitroxyhydraxine also elevated [Ca2+]i. (nih.gov)

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