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N-NITROSODIETHYLAMINE STANDARD IN METHYLENE CHLORIDE



Chemical Properties

CAT No. :

CS-K-00153
CAS Registry No. : 55-18-5
Category : Impurity Standards
Molecular Weight: 102.13
Molecular Formula : C₄H₁₀N₂O



OTHER INFORMATION
IUPAC Name :N,N-diethylnitrous amide
Synonym :Not available
Smileys :CCN(CC)N=O
Appearance :Clear to pale yellow Liquid
Color / Form :Yellow oil
Melting Point :Vapor pressure
Boiling Point :351 °F at 760 mm Hg (NTP, 1992)
Solubility :greater than or equal to 100 mg/mL at 70° F (NTP, 1992)
Density :0.9422 at 68 °F (NTP, 1992)
Chemical Classes :Nitrogen Compounds -> Nitrosamines
Use Classification :Fire Hazards -> Carcinogens, Mutagens, Flammable - 2nd degree, Reactive - 1st degree
Hazard Class :Acute Tox. 3 (100%)
EC Number :200-226-1
UNII :3IQ78TTX1A
NCI Thesaurus Code :C29827
MeSH Entry Terms :Diethylnitrosamine
Other Synonyms :N-NITROSODIETHYLAMINE
Removed Synonyms :DANA
Vapor Pressure : 5.7 mm Hg at 77 °F ; 8.8 mm Hg at 94.1° F (NTP, 1992)
Other Experimental Properties :Specific gravity: 0.9422 at 20 °C/4 °C
Disposal Methods :Generators of waste (equal to or greater than 100 kg/mo) containing this contaminant, EPA hazardous waste number U174, must conform with USEPA regulations in storage, transportation, treatment and disposal of waste.
Toxicity Summary :IDENTIFICATION AND USE: N-nitrosodiethylamine (NDEA) is a yellow oil. It is used as a gasoline and lubricant additive, antioxidant and as a stabilizer in plastics. HUMAN STUDIES: NDEA has been identified as tobacco carcinogen. Short-term exposure of a bronchial epithelial cell line to smoking-equivalent concentrations of tobacco carcinogens including NDEA altered the expression of key proliferation regulatory genes, EGFR, BCL-2, BCL2L1, BIRC5, TP53, and MKI67, similar to that reported in biopsy specimens of pulmonary epithelium described to be preneoplastic lesions. ANIMAL STUDIES: NDEA caused tumors in several species of experimental animals, at several different tissue sites, and by several different routes of exposure. It was carcinogenic in animals exposed perinatally and as adults, causing tumors mainly in the liver, respiratory tract, kidney, and upper digestive tract. Benign and malignant liver tumors occurred in mice, rats, hamsters, guinea pigs, rabbits, dogs, and pigs orally exposed to NDEA. Liver tumors also occurred in rats following inhalation exposure or rectal administration; in mice, rats, and hamsters following intraperitoneal injection; in hamsters, guinea pigs, gerbils, and hedgehogs following subcutaneous injection; in mice following prenatal exposure; in birds following intramuscular injection; and in fish and frogs exposed to NDEA in the tank water. In dogs, exposure to NDEA by stomach tube followed by subcutaneous injection caused cancer of the liver and nasal cavity. Tumors of the lung and upper respiratory tract occurred in mice, rats, hamsters, dogs, and pigs following oral administration of NDEA. Tumors of the kidney occurred in rats following oral, intravenous, or prenatal administration of NDEA. Oral administration also caused kidney tumors in pigs and tumors of the upper digestive tract in mice, rats, and hamsters. The mutagenicity of NDEA was evaluated in Salmonella tester strains TA98, TA100, TA1535, TA1537 and TA1538 (Ames Test), both in the presence and absence of added metabolic activation. NDEA did not cause a reproducible positive response in any of the bacterial tester strains, either with or without metabolic activation. In the presence of liver microsomal fraction from phenobarbital-treated rats, NDEA caused 8-azaguanine-resistant mutants in Chinese hamster V79 cells. NDEA was mutagenic in recessive lethal test in Drosophila melanogaster. The effects of NDEA on sexual development, gametogenesis, and oocyte maturation were studied in Japanese medaka (Oryzias latipes). NDEA reduced the germ cell number dose-dependently during early stages of sexual differentiation in XX larvae, resulting in underdeveloped ovaries in adulthood at low doses. This effect was sex-specific as no such changes were seen in XY larvae. Furthermore, XX and XY larvae that were exposed at a low dose during early life showed a significant reduction in body weight in adulthood. Gonads in sexually immature adult medaka males and females exposed to NDEA were in advanced stages in comparison to that of the controls. ECOTOXICITY STUDIES: NDEA induced oxidative stress and antioxidant defense to zebrafish metabolism system at concentrations over 5 ug/L. After a 42-day exposure, a significant DNA damage was observed in zebrafish liver cells at NDEA concentrations beyond 500 ug/L. Toxic and carcinogenic effects observed in snakes (Phython reticulatus) after lifelong administration of 6, 12, and 24 mg/kg NDEA by gavage at four nightly intervals. Total dose needed to induce tumors was 500-600 mg/kg.
Interactions :OBJECTIVE: The present paper aims to investigate the effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and N-nitrosodiethylamine (DEN) on tumorigenesis and its potential mechanism. METHODS: The potentials of TCDD and DEN in separation or in combination to induce malignant transformation were tested in Balb/c 3T3 cells by using a cell transformation assay method. The possible mechanism of observed effects was studied further by adding a-naphthoflavone (a-NF), a competitive binding agent of TCDD, to the Aryl hydrocarbon receptor (AhR) pathway. The mRNA expressions of Cyp1a1 and Cyp2a5 gene in Balb/c 3T3 cells treated by DEN and TCDD in separation or in combination with or without presence of a-NF were measured with fluorescence quantification RT-PCR technique. RESULTS: The cell transformation frequency (TF) was significantly higher in case of induction with TCDD in combination with DEN, as compared to that with either TCDD or DEN alone. These effects were not inhibited via a-NF. The mRNA expression levels of both Cyp1a1 and Cyp2a5 were enhanced by TCDD treatment alone, but this inducible effect was blocked in cells treated by TCDD and DEN in combination. CONCLUSION: TCDD and DEN had a significant synergistic effect on tumorigenesis when they were used in combination. AhR pathway may not be the key mechanism of this synergistic effect. Thus, it is necessary to further test the potential mechanism involved in cancer development.
Antidoteand Emergency Treatment :Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Organic bases/Amines and related compounds/
Human Toxicity Excerpts :/ALTERNATIVE and IN VITRO TESTS/ The biological effects of only a finite number of tobacco toxins have been studied. Here, /researchers/ describe exposure of cultures of human bronchial epithelial cells to low concentrations of tobacco carcinogens: nickel sulphate, benzo(b)fluoranthene, N-nitrosodiethylamine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). After a 24 hr exposure, EGFR was expressed in cell membrane and cytoplasm, BCL-2 was expressed only in the irregular nuclei of large atypical cells, MKI67 was expressed in nuclei with no staining in larger cells, cytoplasmic BIRC5 with stronger nuclear staining was seen in large atypical cells, and nuclear TP53 was strongly expressed in all cells. After only a 24 hr exposure, cells exhibited atypical nuclear and cytoplasmic features. After a 48-hour exposure, EGFR staining was localized to the nucleus, BCL-2 was slightly decreased in intensity, BIRC5 was localized to the cytoplasm, and TP53 staining was increased in small and large cells. BCL2L1 was expressed in both the cytoplasm and nuclei of cells at 24 and 48 hr exposures. /Researchers/ illustrate that short-term exposure of a bronchial epithelial cell line to smoking-equivalent concentrations of tobacco carcinogens alters the expression of key proliferation regulatory genes, EGFR, BCL-2, BCL2L1, BIRC5, TP53, and MKI67, similar to that reported in biopsy specimens of pulmonary epithelium described to be preneoplastic lesions.
Non Human Toxicity Excerpts :/LABORATORY ANIMALS: Acute Exposure/ The acute necrogenic effects of N-nitrosodiethylamine (NDEA) on nasal tissues of female Sprague-Dawley rats and golden Syrian hamsters were determined. Rats and hamsters were given a single ip dose of 0, 10, 20, 40, or 80 mg NDEA/kg bw. After 24 hr, the rats and hamsters were killed and tissues were collected. Sections of nasal cavity and liver were evaluated histologically. All doses of NDEA caused inhibition of glycoprotein synthesis in cells of Bowman's glands in the olfactory region of rats and hamsters as determined by the loss of Alcian blue-periodic acid-Schiff staining material. Glycoprotein synthesis in other glands including the lateral nasal glands, maxillary glands, medial nasal glands, and the acinous glands near the vomeronasal organ was not affected by NDEA. Necrosis of Bowman's glands in the olfactory region of the nasal cavity occurred in rats given 20, 40, or 80 mg NDEA/kg bw whereas the same cells were not necrotic in hamsters given NDEA. The results demonstrate the unique susceptibility of cells of the Bowman's glands to the toxic effects of NDEA given ip and indicate that nasal tissues of the rat are more susceptible to the necrogenic effects of NDEA than those of the hamster.
Exact Mass :102.079312947
InChI :InChI=1S/C4H10N2O/c1-3-6(4-2)5-7/h3-4H2,1-2H3
InchIKey :WBNQDOYYEUMPFS-UHFFFAOYSA-N
Canonical SMILES :CCN(CC)N=O
Isomeric SMILES :CCN(CC)N=O
Hazard Summary :Danger of cutaneous absorption; [MAK] May cause irritation; Effects in high-dose animal studies include fatty liver degeneration; [MSDSonline]
Product Description :N-nitrosodiethylamine is a nitrosamine that is N-ethylethanamine substituted by a nitroso group at the N-atom. It has a role as a mutagen, a hepatotoxic agent and a carcinogenic agent.
Custom Duty : Applicable
Port of Loading : Canada
Expected Dispatch : 15-Aug-2022
Taxes : Not Applicable
Refund Policy : 30-days money back
Custom Duty : Applicable
Port of Loading : Canada
Expected Dispatch : 15-Aug-2022
Taxes : Not Applicable
Refund Policy : 30-days money back


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