Cyanamide
Vicia
Acetaldehyde
Aldehyde Dehydrogenase
The effect of inhibition of aldehyde dehydrogenase on nasal uptake of inspired acetaldehyde. (1/62)
At exposure concentrations of 750 ppm or more, acetaldehyde is a rodent inhalation carcinogen that induces nasal tumors. Aldehyde dehydrogenase (ALDH) is thought to be an important detoxifying enzyme for aldehydes. Although nasal tissues express ALDH, the importance of this enzyme relative to delivered dosage rates at high-inspired concentrations is not well defined. To provide such information, uptake of inspired acetaldehyde was measured at an inspiratory flow rate that approximated the minute ventilation rate in the surgically isolated nasal cavity of F 344 rats pretreated with either saline (control) or the ALDH inhibitor, cyanamide (10 mg/kg s.c.). ALDH activities (substrate concentration 3 times the K(m)) in anterior (respiratory mucosa) and posterior (olfactory mucosa) nasal tissues averaged 160 and 210 nmol/min), respectively, in control animals (total activity 370 nmol/min), compared to 60 and 80 nmol/min, respectively, in cyanamide-pretreated rats (p < 0.05), indicating that approximately 60% inhibition was obtained. Nasal uptake was measured at 3 inspired concentrations: 10, 300, and 1500 ppm. At these concentrations, acetaldehyde uptake efficiency averaged 54, 37, and 34% in saline-pretreated rats, respectively (p < 0.05). In absolute terms, the delivered dosage rates at these exposure concentrations averaged 21, 420, and 1990 nmol/min. The concentration dependence on uptake suggests a saturable process was involved. At inspired concentrations of 300 ppm or more, the delivered dosage rates exceeded the measured specific activity for nasal ALDH of 370 nmol/min. Cyanamide pretreatment abolished the concentration dependence. Specifically, uptake efficiencies in cyanamide-pretreated rats averaged 30, 27, and 31% at inspired concentrations of 10, 300, and 1500 ppm, respectively (p > 0.05); delivered dosage rates were 12, 310, and 1780 nmol/min. Thus, cyanamide pretreatment reduced nasal-delivered dosage rates at inspired concentrations of 10, 300, and 1500 ppm, respectively by 9, 110, and 210 nmol/min, values that correspond well with the total nasal ALDH activity of 370 nmol/min. In toto, these results suggest that inspired acetaldehyde is metabolized in situ by ALDH, but at exposure concentrations of 300 ppm or greater, the delivered dosage rate may equal or exceed the capacity of this enzyme. (+info)The transcriptional and DNA binding activity of peroxisome proliferator-activated receptor alpha is inhibited by ethanol metabolism. A novel mechanism for the development of ethanol-induced fatty liver. (2/62)
Fatty acids are ligands for the peroxisome proliferator-activated receptor alpha (PPAR alpha). Fatty acid levels are increased in liver during the metabolism of ethanol and might be expected to activate PPAR alpha. However, ethanol inhibited PPAR alpha activation of a reporter gene in H4IIEC3 hepatoma cells expressing alcohol-metabolizing enzymes but not in CV-1 cells, which lack these enzymes. Ethanol also reduced the ability of the PPAR alpha ligand WY14,643 to activate reporter constructs in the hepatoma cells or cultured rat hepatocytes. This effect of ethanol was abolished by the alcohol dehydrogenase inhibitor 4-methylpyrazole and augmented by the aldehyde dehydrogenase inhibitor cyanamide, indicating that acetaldehyde was responsible for the action of ethanol. PPAR alpha/retinoid X receptor extracted from hepatoma cells exposed to ethanol or acetaldehyde bound poorly to an oligonucleotide containing peroxisome proliferator response elements. This effect was also blocked by 4-methylpyrazole and augmented by cyanamide. Furthermore, in vitro translated PPAR alpha exposed to acetaldehyde failed to bind DNA. Thus, ethanol metabolism blocks transcriptional activation by PPAR alpha, in part due to impairment of its ability to bind DNA. This effect of ethanol may promote the development of alcoholic fatty liver and other hepatic consequences of alcohol abuse. (+info)Ethanol potentiates hypoxic liver injury: role of hepatocyte Na(+) overload. (3/62)
Centrilobular hypoxia has been suggested to contribute to hepatic damage caused by alcohol intoxication. However, the mechanisms involved are still poorly understood. We have investigated whether alterations of Na(+) homeostasis might account for ethanol-mediated increase in hepatocyte sensitivity to hypoxia. Addition of ethanol (100 mmol/l) to isolated rat hepatocytes incubated under nitrogen atmosphere greatly stimulated cell death. An increase in intracellular Na(+) levels preceded cell killing and Na(+) levels in hepatocytes exposed to the combination of ethanol and hypoxia were almost twice those in hypoxic cells without ethanol. Na(+) increase was also observed in hepatocytes incubated with ethanol in oxygenated buffer. Ethanol addition significantly lowered hepatocyte pH. Inhibiting ethanol and acetaldehyde oxidation with, respectively, 4-methylpyrazole and cyanamide prevented this effect. 4-methylpyrazole, cyanamide as well as hepatocyte incubation in a HCO(3)(-)-free buffer or in the presence of Na(+)/H(+) exchanger blocker 5-(N,N-dimethyl)-amiloride also reduced Na(+) influx in ethanol-treated hepatocytes. 4-methylpyrazole and cyanamide similarly prevented ethanol-stimulated Na(+) accumulation and hepatocyte killing during hypoxia. Moreover, ethanol-induced Na(+) influx caused cytotoxicity in hepatocytes pre-treated with Na(+), K(+)-ATPase inhibitor ouabain. Also in this condition 4-methylpyrazole and 5-(N,N-dimethyl)-amiloride decreased cell killing. These results indicate that ethanol can promotes cytotoxicity in hypoxic hepatocytes by enhancing Na(+) accumulation. (+info)Acetaldehyde, a metabolite of ethanol, activates the hypothalamic-pituitary-adrenal axis in the rat. (4/62)
Cyanamide is a potent inhibitor of aldehyde dehydrogenase (ALDH: EC 1.2.1.3) used in the treatment of alcoholics. In the presence of ethanol, cyanamide causes an accumulation of acetaldehyde, a highly toxic metabolite of ethanol, with unpleasant side-effects. A similar accumulation is seen in some Oriental people with low ALDH activity. We have investigated the effects of ethanol and cyanamide administration on the activation of the hypothalamic-pituitary-adrenal (HPA) axis using in situ hybridization histochemistry and radioimmunoassay. Ethanol plus cyanamide resulted in a significant increase in corticotrophin-releasing factor and arginine vasopressin mRNA in the paraventricular nucleus, and pro-opiomelanocortin mRNA in the anterior pituitary. Plasma corticosterone concentrations were also significantly elevated following ethanol plus cyanamide administration. The blood concentration of acetaldehyde in the ethanol plus cyanamide group increased significantly. These results suggest that acetaldehyde, induced by blocking ethanol metabolism, is able to activate the HPA axis operating through a central mechanism. (+info)Cholinergic nerves mediate acetaldehyde action in the gastrointestinal tract. (5/62)
The regulation mechanism of inhibition of intestinal ethanol absorption induced by high acetaldehyde (AcH) concentration in blood was investigated. We used atropine (AT), atropine methylbromide (ATMB), pirenzepine (PI), bethanechol (BE) and pilocarpine (PL) with or without cyanamide (CY; a potent inhibitor of aldehyde dehydrogenase, which induces high AcH concentration in blood). The K(a) (absorption rate constant) value after the CY-alone pretreatment was significantly lower than that in controls. In the high AcH-induced cases, the values of K(a) in AT and ATMB pretreatments were similar to controls, but the value of K(a) in PI pretreatment was lower than that in controls. The values of K(a) in the case of BE pretreatment with and without high AcH levels were lower than in controls. The K(a) value in the PL with CY was significantly lower than that with CY alone. However, its action was blocked by ATMB pretreatment. These results suggest that high blood AcH concentrations inhibit intestinal ethanol absorption through the peripheral cholinergic nerves via muscarinic receptors, except for the muscarinic M(1) receptor, compared to other subtypes of muscarinic receptors. (+info)Pesticide-related illnesses associated with the use of a plant growth regulator--Italy, 2001. (6/62)
During January-February 2001, eight cases of acute illness in the county of Ragusa, Italy, were reported to the Italian National Institute for Health (INIH) by the Milan Poison Control Center (MPCC) and were attributed to exposure to Dormex, a plant growth regulator with hydrogen cyanamide as the active ingredient. These cases were identified during a pilot project for acute pesticide-related illness surveillance. Subsequent active case finding at health-care clinics by the Ragusa Occupational Health Unit identified six additional cases. MPCC identified nine cases in other areas of Italy. Of the 23 cases of acute illness, 22 resulted from occupational exposure during mixing and/or applying of Dormex, and one was from unintentional ingestion. This report summarizes the investigation of these cases, which implicates a pesticide as the causative agent and demonstrates the usefulness of surveillance for detecting pesticide-related illnesses. (+info)Combined calcium carbimide and ethanol treatment induces high blood acetaldehyde levels, myocardial apoptosis and altered expression of apoptosis-regulating genes in rat. (7/62)
The effects of ethanol and ethanol-derived acetaldehyde on rat myocardial apoptosis and expression of genes involved in the regulation of apoptosis and cell cycle arrest were studied. Combined ethanol and calcium carbimide treatment for 2, 5 or 8 days (E + CC) markedly increased blood acetaldehyde levels. Cytosolic DNA fragmentation was quantified in the 5-day treatment group. Increased amount of DNA-fragmentation, reflecting increased apoptosis, was evident in the E + CC group (23% increase compared to controls). mRNA levels of genes regulating apoptosis were measured by using quantitative PCR in the 2- and 8-day treatment groups. In the 2-day treatment group, p21 gene expression was increased by 25% and bax/bcl-2 mRNA ratio by 57% in E + CC, compared to the control, group. In the 8-day treatment group, p21 mRNA level was 24% lower, p53 mRNA level was 15% higher (P < 0.005), and bcl-2 mRNA level 36% higher in E + CC-treated, compared to the control, group. Interestingly, both ethanol and calcium carbimide treatments alone increased bax mRNA levels, as compared to the control group at 2 and 8 days. These results indicate that acetaldehyde might regulate the expression of apoptosis-linked genes and that apoptosis of myocardial cells may be involved in the development of alcoholic heart disease. (+info)Modelling kiwifruit budbreak as a function of temperature and bud interactions. (8/62)
This paper presents two models of budbreak on canes of 'Hayward' kiwifruit (Actinidia deliciosa). A conventional 'chill unit' (CU) type model is compared with an alternative 'loss of potential' (LOP) approach, which assumes that the number of buds developing in spring depends on climate and node position-dependent bud-to-bud interactions that vary in duration and intensity. Both models describe how temperature, and application of a dormancy-breaking chemical, determine the overall amount of budbreak for whole canes. However, the LOP model does so by describing patterns of budbreak along canes. To do this, the cumulative influence of distal neighbours is assumed to cause a progressive fall in the capacity for bud development over the autumn-winter period, an influence that gets stronger as temperature rises. The LOP model also assumes that the rate of decline varies along the cane, as a function of some inherent bud property. These two factors mean that buds towards the base of the cane break less often under the suppressive influence of distal neighbours, while low temperature ('chilling') increases budbreak by diminishing the intensity of suppression relative to bud development rate. Under this scenario, dormancy-breaking chemicals (such as hydrogen cyanamide, HC) enhance budbreak by diminishing the duration of suppression. Models were calibrated using daily temperature series and budbreak proportion data from a multi-year regional survey, and were then tested against independent data sets. Both models were run from a fixed start date until the time budbreak was almost complete, or until a standard date. The fitted models described 87 % of variation in amount of budbreak due to site, year, HC and node position effects in the original data set. Results suggest that the correlation between chilling and the amount of budbreak can be interpreted as a population-based phenomenon based on interaction among buds. (+info)Cyanamide is a chemical compound that is used in various industrial applications, including the production of fertilizers, dyes, and plastics. In the medical field, cyanamide has been used as a treatment for certain types of cancer, such as bladder cancer and head and neck cancer. It works by inhibiting the growth of cancer cells and promoting their death. However, the use of cyanamide as a cancer treatment is not widely accepted and is not commonly used in modern medicine. It is important to note that cyanamide can be toxic and can cause serious side effects, including nausea, vomiting, and respiratory problems. Therefore, it is only used under the supervision of a qualified healthcare professional.
Acetaldehyde is a chemical compound that is produced naturally in the body during the metabolism of alcohol and certain other substances. It is also used in the production of a variety of chemicals and industrial products, including plastics, resins, and perfumes. In the medical field, acetaldehyde is sometimes used as a diagnostic tool to help identify certain types of liver disease. It is also used as a treatment for certain types of cancer, such as head and neck cancer, by helping to kill cancer cells or slow their growth. However, acetaldehyde is also a toxic substance that can cause a range of health problems, including nausea, vomiting, headache, and dizziness. At high levels, it can be fatal. As a result, exposure to acetaldehyde should be avoided whenever possible, and steps should be taken to limit its production and release into the environment.
Aldehyde dehydrogenase (ALDH) is an enzyme that plays a crucial role in the metabolism of aldehydes, which are toxic compounds that can be produced during the breakdown of certain drugs, alcohol, and other substances. ALDH catalyzes the oxidation of aldehydes to their corresponding carboxylic acids, which are less toxic and can be further metabolized by other enzymes in the body. In the medical field, ALDH is important for detoxifying the body and preventing the accumulation of toxic aldehydes. Deficiency in ALDH can lead to a condition called aldehyde dehydrogenase deficiency, which can cause sensitivity to certain drugs and alcohol, as well as other health problems. ALDH is also a target for the development of new drugs for the treatment of various diseases, including cancer, neurodegenerative disorders, and alcohol addiction.
In the medical field, diynes are a class of organic compounds that contain two carbon-carbon triple bonds. They are typically unsaturated hydrocarbons with a general formula of C2nH2n-2, where n is an integer greater than or equal to 3. Diynes are often used as precursors for the synthesis of other organic compounds, such as polymers, pharmaceuticals, and materials for electronic devices. They can also be used as ligands in metal complexes, and as building blocks for the synthesis of complex organic molecules. In some cases, diynes can be toxic or carcinogenic, and their use in the medical field is therefore regulated. For example, certain diynes have been used as contrast agents in magnetic resonance imaging (MRI), but their use is limited due to potential toxicity and other safety concerns.
In the medical field, "alcohol deterrents" refer to substances or methods used to discourage or prevent excessive alcohol consumption. These deterrents can be used in a variety of settings, including hospitals, clinics, and rehabilitation centers, as well as in the community. Alcohol deterrents can take many forms, including: 1. Education and counseling: This involves providing information about the risks and consequences of excessive alcohol consumption, as well as offering support and guidance to help individuals make healthier choices. 2. Medications: There are several medications available that can help reduce alcohol cravings and withdrawal symptoms, making it easier for individuals to quit or reduce their alcohol use. 3. Behavioral interventions: These involve working with individuals to identify and change the behaviors and thought patterns that contribute to their alcohol use. 4. Environmental modifications: This involves making changes to the individual's environment to reduce the availability and accessibility of alcohol, such as removing alcohol from the home or limiting access to alcohol in social settings. Overall, alcohol deterrents are an important tool in the prevention and treatment of alcohol use disorders, helping individuals to reduce their alcohol consumption and improve their overall health and well-being.
Cyanamide
Calcium cyanamide
Cyanamide hydratase
History of the Haber process
Calcium carbide
Carbide lamp
Acetylene
2-Cyanoguanidine
Calcium cyanide
Cyanuric bromide
Isodiazomethane
Frank-Caro process
December 1909
Sydney Francis Ashby
Carbodiimide
Robert Smock
Aza-Cope rearrangement
Nitrosyl cyanide
Akabori amino-acid reaction
List of interstellar and circumstellar molecules
Graphitic carbon nitride
CA1 (gene)
Trostberg
George Owen Knapp
Diazomethane
Pimagedine
Melamine
Bettina Lotsch
Carbon compounds
Denka
Cyanamide - Wikipedia
Cyanamide, dimethyl
Mamdouh Fawzy Ahmed Mohamed - cyanamide;
where to buy Dormex (Hydrogen Cyanamide 49% AS) - FandaChem
Air Contaminants Update Project | NIOSH | CDC
Observed Interstellar Molecular Microwave Transitions, Table 1 | NIST
Oral Manifestations of Drug Reactions: Overview, Xerostomia, Swelling
Oral Manifestations of Drug Reactions: Overview, Xerostomia, Swelling
NIOSHTIC-2 Search Results - Basic View
ISO 5314:1981 - Fertilizers - Determination of ammoniacal nitrogen content - Titrimetric method after distillation
Periodic Table of Elements: Los Alamos National Laboratory
Agronomy | Free Full-Text | Supplementary LED Interlighting Improves Yield and Precocity of Greenhouse Tomatoes in the...
HeteroCycles
The formation of urea in space - I. Ion-molecule, neutral-neutral, and radical gas-phase reactions | Astronomy & Astrophysics ...
Publikationen • AG Dau • Physik
Pathology Outlines - Drug / toxin induced hepatitis (DILI)-general
Iodine I 131 Lym-1 Monoclonal Antibody - CheckOrphan
H2O + CaCN2 → CaCO3 + NH3 | Equation Balance
Does rooster come back in the ranch season 8? - TipsFolder.com
An Agricultural Testament - Albert Howard - 4
Label of Liquid Methylene Urea
Project Reports & Profiles » Business Ideas: 40 - 50 Lakhs (Plant and Machinery): Selected Project Profiles for Entrepreneurs,...
Iron(II) oxide - Wikipedia
2-Nitro-4-(Propylthio)-Aniline - Axios Research
Magnus
CCCBDB bad vibrational frequency prediction
Sucralose|Galanthamine|Huperzine A|Solanesol--Shanghai Trustin IMP&EXP Co.,Ltd.
Hydrogen Cyanamide1
- Update: hydrogen cyanamide--related illnesses - Italy, 2002-2004. (cdc.gov)
Calcium3
- Derivatives of this compound are also referred to as cyanamides, the most common being calcium cyanamide (CaCN2). (wikipedia.org)
- Cyanamide is produced by hydrolysis of calcium cyanamide, which in turn is prepared from calcium carbide via the Frank-Caro process. (wikipedia.org)
- Sodium cyanide can also be prepared by heating sodium amide with carbon or by melting sodium chloride and calcium cyanamide together in an electric furnace (Hartung 1982). (cdc.gov)
Urea2
- Water, hydrogen sulfide, and hydrogen selenide react with cyanamide to give urea, thiourea, and selenourea, respectively: H2NCN + H2E → H2NC(E)NH2 (E = O, S, Se) In this way, cyanamide behaves as a dehydration agent and thus can induce condensation reactions. (wikipedia.org)
- It is applicable only in the absence of urea or its derivatives, of cyanamide and of organic nitrogenous compounds. (iso.org)
Dormex1
- Cyanamide, under the trade name Dormex, is a common agricultural rest-breaking agent applied in spring to stimulate uniform opening of buds, early foliation and bloom. (wikipedia.org)
Compounds1
- The main reaction exhibited by cyanamide involves additions of compounds containing an acidic proton. (wikipedia.org)
Organic1
- Cyanamide is an organic compound with the formula CN2H2. (wikipedia.org)
Reaction2
- A convenient method for the preparation of secondary amines which are not contaminated with primary or tertiary amines is the reaction of cyanamide with alkyl halides to N,N-dialkylcyanamides which can easily be hydrolyzed to dialkylamines and then decarboxylated. (wikipedia.org)
- A guanidino group is introduced by reaction of cyanamide with sarcosine In the industrial synthesis of creatine: This synthesis route mostly avoids problematic impurities like chloroacetic acid, iminodiacetic acid, or dihydrotriazine that occur in other routes. (wikipedia.org)
Synthesis1
- Cyanamide is also used in the synthesis of other pharmaceutical drugs including tirapazamine, etravirine, revaprazan, and dasantafil. (wikipedia.org)
Carbon1
- Cyanamide can be regarded as a functional single carbon fragment which can react as an electrophile or nucleophile. (wikipedia.org)
Formula1
- Cyanamide exists as two tautomers, one with the connectivity N≡C-NH2 and the other with the formula HN=C=NH ("carbodiimide" tautomer). (wikipedia.org)
Water1
- The cyanamide anion has the character of a pseudo chalcogen, cyanamide can therefore be regarded as analogue to water or hydrogen sulfide. (wikipedia.org)
Calcium salt1
- It often occurs as the calcium salt, sometimes also referred to as cyanamide. (nih.gov)
Amines1
- A convenient method for the preparation of secondary amines which are not contaminated with primary or tertiary amines is the reaction of cyanamide with alkyl halides to N,N-dialkylcyanamides which can easily be hydrolyzed to dialkylamines and then decarboxylated. (wikipedia.org)
Disulfiram3
- Disulfiram also causes hepatitis, but there have been no comparative studies of effects of cyanamide and disulfiram on liver function. (nih.gov)
- Among the subjects, 222 patients received cyanamide treatment (a daily dose of 70 mg) without a history of disulfiram treatment, and 186 received disulfiram (a daily dose of 200 mg) without a history of cyanamide treatment. (nih.gov)
- In patients who took cyanamide, the ALT levels were significantly higher at 4 and 12 weeks than in those who took disulfiram. (nih.gov)
Hydrogen8
- The cyanamide anion has the character of a pseudo chalcogen, cyanamide can therefore be regarded as analogue to water or hydrogen sulfide. (wikipedia.org)
- Hydrogen cyanamide* is used in agriculture as a plant growth regulator and is applied to many deciduous plants to stimulate uniform budbreak after dormancy, resulting in uniform flowering and maturity. (cdc.gov)
- Hydrogen cyanamide is highly toxic, and adverse health effects from contact include severe irritation and ulceration of the eyes, skin, and respiratory tract ( 1,2 ). (cdc.gov)
- After Dormex ® (Degussa AG, Trostberg, Germany), a pesticide product containing hydrogen cyanamide (49% by weight), was introduced in Italy in 2000, a total of 23 cases of acute illness associated with exposure to this chemical were identified in early 2001 ( 3 ). (cdc.gov)
- This report describes 28 additional cases of hydrogen cyanamide--related illness that occurred during 2002--2004, 14 of which occurred after sales resumed. (cdc.gov)
- These illnesses suggest that the preventive measures adopted in Italy in 2003 to protect workers using hydrogen cyanamide are inadequate. (cdc.gov)
- Workers exposed to hydrogen cyanamide should be provided adequate information, training, personal protective equipment (PPE), and engineering controls. (cdc.gov)
- A total of 28 hydrogen cyanamide--related illnesses were identified during 2002--2004. (cdc.gov)
Derivatives1
- Derivatives of this compound are also referred to as cyanamides, the most common being calcium cyanamide (CaCN2). (wikipedia.org)
Uniform1
- Cyanamide, under the trade name Dormex, is a common agricultural rest-breaking agent applied in spring to stimulate uniform opening of buds, early foliation and bloom. (wikipedia.org)
Temperatures1
- Computer Simulation Investigation of the Adsorption of Cyanamide on Amorphous Ice at Low Temperatures , JOURNAL OF PHYSICAL CHEMISTRY C 124: (19) pp. 10615-10626. (doktori.hu)
Effects1
- The development of hepatocyte cytoplasmic inclusions in both our cases could be related to medication effects, because similar inclusions were reported in patients using cyanamide. (elsevierpure.com)
Patients1
- We used 11 C-CNS 5161 [ N -methyl-3(thyomethylphenyl)cyanamide] positron emission tomography, a marker of activated N -methyl- D -aspartate receptor ion channels, to compare in vivo glutamate function in parkinsonian patients with and without levodopa-induced dyskinesias. (medscape.com)
Treatment1
- The hair-loss treatment minoxidil and the anthelmintics albendazole, flubendazole, and mebendazole feature 2-aminoimidazole substructures derived from cyanamide. (wikipedia.org)