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At least 19 recordsLinked to original sources
PubMed1986

Transport of dimethylamine, a precursor of nitrosodimethylamine, into stomach of ferret and dog.

Dimethylamine is important because it is a precursor of nitrosodimethylamine, a suspected carcinogen in man. Significant quantities of dimethylamine and nitrite are found in gastric fluid, and conditions in the stomach are favorable for nitrosodimethylamine formation. Little is known about the origins of dimethylamine in gastric fluid. Studies were performed to determine whether dimethylamine can be transported from blood to gastric fluid. There was no diurnal variation of the dimethylamine content in gastric fluid or blood from untreated dogs. We administered 50 mg/kg dimethylamine i.v. to dogs and ferrets and collected blood and gastric fluid samples at timed intervals. In both species we observed similar kinetics of dimethylamine distribution into biologic fluids. Dimethylamine concentrations in blood and gastric fluid rose rapidly during the first minutes after treatment. Blood dimethylamine concentrations peaked within 30 min after the dose (rising from 10 to 430 nmol/ml in the dogs, and from 30 to 430 nmol/ml in the ferrets). Dimethylamine concentrations in blood slowly decreased thereafter. Gastric fluid dimethylamine concentrations continued to rise for 3 h after the dose (from 40 to 540 nmol/ml in the dogs, and from 40 to 1056 nmol/ml in the ferrets). Gastric fluid dimethylamine remained elevated for more than 5 h. Between 1 h and 5 h after treatment, gastric fluid dimethylamine concentrations were significantly higher than blood dimethylamine concentrations (by greater than 2.5 X). In gastric fluid from control animals, dimethylamine concentration exceeded monomethylamine concentration, which in turn was higher than trimethylamine concentration. Administration of dimethylamine transiently increased gastric fluid monomethylamine content, but had little effect upon trimethylamine concentration. These data demonstrate that dimethylamine is efficiently transported from blood into gastric fluid.

Animals↗
PubMedDate not supplied

Oleamidopropyl dimethylamine.

The cationic emulsifier oleamidopropyl dimethylamine has been responsible for many cases of cosmetic sensitisation in The Netherlands. Of 119 patients with proven cosmetic-related allergic contact dermatitis, 13 (11%) were allergic to oleamidopropyl dimethylamine. The clinical data of 12 patients, all sensitised by one particular baby body lotion containing 0.3% of the emulsifier, are presented. The cross-reaction pattern of oleamidopropyl dimethylamine was investigated by patch testing 13 patients allergic to the emulsifier with a series of related amideamine type emulsifiers. Most cross-reactions were observed to ricinoleamidopropyl dimethylamine lactate and tallowamidopropyl dimethylamine (11 patients, 85%). 9 patients (of 12 tested: 75%) reacted to lauramidopropyl dimethylamine and 6 (46%) to myristamidopropyl dimethylamine. It is concluded that the presence of oleamidopropyl dimethylamine in a concentration of 0.3% in stay-on cosmetics, especially when applied to damaged skin and/or the periorbital area, bears a definite risk of the induction and elicitation of contact allergic reactions.

Cosmetics↗
PubMed1988

Cross-reaction pattern of the cationic emulsifier oleamidopropyl dimethylamine.

13 patients allergic to the cationic emulsifier oleamidopropyl dimethylamine were tested with a series of related amide-amine type surfactants in order to investigate its cross-reaction pattern. With 1 exception, all patients reacted to at least 4 of the test materials. Most reactions were observed to ricinoleamidopropyl dimethylamine lactate and tallowamidopropyl dimethylamine (11 patients, 85%); 9 patients (of 12 tested, 75%) reacted to lauramidopropyl dimethylamine and 6 (46%) to myristamidopropyl dimethylamine. A certain pattern of cross-reactivity was recognised.

Adolescent↗
PubMed1987

Effect of ascorbic acid on the hepatotoxicity due to the daily intake of nitrate, nitrite and dimethylamine.

It is known that nitrates, nitrites and dimethylamine may react in the gastro-intestinal tract synthesizing the powerful hepatotoxic and carcinogenic dimethylnitrosamine. The purpose of this study was to investigate hepatotoxicity due to the daily intake of nitrates and nitrites administered to rats during 14 weeks together with dimethylamine in drinking water, and to evaluate the protecting effect of ascorbic acid against the hepatotoxicity of the presumably endogenous formed dimethylnitrosamine. The toxicity criteria studied were weight of liver (absolute and relative), free and total bilirubin, alkaline phosphatase and pyruvic glutamic transaminase, all in the form of serum, and histopathologic tests of the liver. The results gave evidence of hepatotoxicity induced by the intake of nitrate, nitrite and dimethylamine all together, and not through the only intake of nitrate or nitrite or of amine. Daily doses of ascorbic acid [(211 +/- 40) and (18 +/- 4) mg/kg] seemed to hinder hepatotoxicity according to the criteria under investigation.

Alanine Transaminase↗
PubMed1990

The measurement of dimethylamine, trimethylamine, and trimethylamine N-oxide using capillary gas chromatography-mass spectrometry.

We have developed a method for measuring dimethylamine (DMA), trimethylamine (TMA), and trimethylamine N-oxide (TMAO) in biological samples using gas chromatography with mass spectrometric detection. DMA, TMA, and TMAO were extracted from biological samples into acid after internal standards (labeled with stable isotopes) were added. p-Toluenesulfonyl chloride was used to form the tosylamide derivative of DMA. 2,2,2-Trichloroethyl chloroformate was used to form the carbamate derivative of TMA. TMAO was reduced with titanium(III) chloride to form TMA, which was then analyzed. The derivatives were chromatographed using capillary gas chromatography and were detected and quantitated using electron ionization mass spectrometry (GC/MS). Derivative yield, reproducibility, linearity, and sensitivity of the assay are described. The amounts of DMA, TMA, and TMAO in blood, urine, liver, and kidney from rats and humans, as well as in muscle from fishes, were determined. We also report the use of this method in a pilot study characterizing dimethylamine appearance and disappearance from blood in five human subjects after ingesting [13C]dimethylamine (0.5 mumol/kg body wt). The method we describe was much more reproducible than existing gas chromatographic methods and it had equivalent sensitivity (detected 1 pmol). The derivatized amines were much more stable and less likely to be lost as gases when samples were stored. Because we used GC/MS, it was possible to use stable isotopic labels in studies of methylamine metabolism in humans.

Animals↗
PubMed1976

Microbial formation and degradation of dimethylamine.

Dimethylamine was formed from trimethylamine in soils of different pH values. The rate of disappearance of the secondary amine from soil was affected by pH and was markedly reduced under anaerobiosis. The accumulation of dimethylamine in cultures of Micrococcus sp. provided with trimethylamine depended on the nitrogen sources available to the bacterium but was not greatly influenced by the C-N ratio of the medium. Dimethylamine and nitrite accumulated in large amounts at pH 6.0 to 8.0 in cultures containing the tertiary amine and nitrate, but dimethylnitrosamine was apparently not produced.

Anaerobiosis↗
PubMed1985

Effects of methyl linoleate hydroperoxide and hydrogen peroxide on N-nitrosation of dimethylamine.

The effects of methyl linoleate hydroperoxide and hydrogen peroxide on the N-nitrosation of dimethylamine were investigated. Hydrogen peroxide inhibited the formation of N-nitrosodimethylamine by the reaction of dimethylamine and nitrite in citrate buffer (pH 3-5). The inhibitory effect was due to the loss of available nitrite by quantitative conversion into nitrate. The formation of N-nitrosodimethylamine from the reaction of dimethylamine and nitrous acid in chloroform was effectively inhibited by methyl linoleate hydroperoxide. The inhibitory effect of the hydroperoxide was much greater than that of methyl linoleate. The loss of nitrous acid from the reaction mixture was due to the conversion of nitrous acid into nitric acid and the formation of two adducts, both of which contained nitrogen and had peroxide and carbonyl or carbonyl-liberating functions. It is suggested that unsaturated fatty acids and lipid hydroperoxides are effective inhibitors of nitrosamine formation.

Chromatography, Thin Layer↗
PubMed1988

Fecal methylamine and dimethylamine in chronic renal failure.

Determinations of methylamine and dimethylamine in the fecal samples from normal subjects (n = 22), nonhemodialysis patients (n = 10), and hemodialysis patients (n = 14) with chronic renal failure have been made by high-performance liquid chromatography of their 2,4-dinitrophenyl derivatives. Fecal methylamine level was significantly lower in the normal group than in the nonhemodialysis group (P less than 0.05) and in the hemodialysis group (P less than 0.05). The mean dimethylamine value of the hemodialysis group was significantly higher than that of the nonhemodialysis group (P less than 0.01) and that of the normal group (P less than 0.005). The method has also been applied to the determination of the two amines in the fecal samples from two patients with leukemia who had been isolated and sterilized in the laminar air flow rooms. Preliminary in vitro experiments were given of the possible pathway for the production of these amines by the incubation of normal fecal samples with added creatinine.

Chromatography, High Pressure Liquid↗
PubMed1985

The toxicity of dimethylamine in F-344 rats and B6C3F1 mice following a 1-year inhalation exposure.

Dimethylamine is a widely used commodity chemical, for which there are few chronic toxicity data. Male and female F-344 rats and B6C3F1 mice were exposed by inhalation to 0, 10, 50, or 175 ppm dimethylamine (DMA) for 6 hr/day, 5 days/week for 12 months. Groups of 9-10 male and female rats and mice were necropsied after 6 and 12 months of exposure. No male mice were sacrificed at 12 months due to a high incidence of early deaths in that group. The mean body weight gain of rats and mice exposed to 175 ppm DMA was depressed to approximately 90% of control after 3 weeks of exposure. The only other treatment-related changes were concentration-related lesions in the nasal passages. Two distinct locations in the nose were affected: the respiratory epithelium in the anterior nasal passages, and the olfactory epithelium, especially that lining the anterior dorsal meatus. There was focal destruction of the anterior nasoturbinate and nasal septum, local inflammation, and focal squamous metaplasia of the respiratory epithelium in rats and mice. Mild goblet cell hyperplasia was observed only in rats. The olfactory epithelium exhibited extensive loss of sensory cells with less damage to sustentacular cells. There was also loss of olfactory nerves, hypertrophy of Bowman's glands, and distension of the ducts of these glands by serocellular debris in regions underlying degenerating olfactory epithelium. At the 175-ppm exposure level, rats had more extensive olfactory lesions than mice, with hyperplasia of small basophilic cells adjacent to the basement membrane being present in rats but not mice. After 12 months of exposure to 10 ppm DMA, minimal loss of olfactory sensory cells and their axons in olfactory nerve bundles was observed in the nasal passages of a few rats and mice. These results indicate that the olfactory sensory cell is highly sensitive to the toxic effects of DMA, with minor lesions being produced in rodents even at the current threshold limit value of 10 ppm.

Air Pollutants↗
PubMed1976

Relevance of dimethylamine to mechanism studies of DIC (DTIC, NSC 45388).

Monolayer cultures of Chinese hamster ovary (CHO) cells take up the photo-decomposition products of DIC more readily than DIC itself. Dimethylamine, an immediate product of this degradative pathway, can ultimately become associated with the DNA, RNA, and protein of the cells as demonstrated by selective enzymatic degradation of macromolecules and isopycnic centrifugation. The relevance of these observations to mechanism studies of DIC is discussed.

Animals↗
PubMed1987

Effects of acute and chronic dimethylamine exposure on the nasal mucociliary apparatus of F-344 rats.

Dimethylamine (DMA) is a highly water soluble gas with many industrial applications. Male F-344 rats were exposed to 175 ppm DMA 6 hr per day for 1, 2, 4, or 9 days or 2 years. Gross changes in nasal structure were recorded, effects of DMA on the mucociliary apparatus were assessed using video analysis, and tissues were evaluated for histopathology. In vitro nasal mucociliary flow patterns, mucus flow rates, and ciliary activity were studied and recorded for video motion analysis. There were distinct and generally consistent differences in the shape of the naso-, maxillo-, and ethmoid turbinates between young and old animals. Acute and chronic DMA exposures resulted in erosion of the anterior margins of the naso- and maxilloturbinates and fenestration of the adjacent septum. Ciliastasis and mucostasis were observed only on the anteromedial aspect of the maxilloturbinate. In the chronically exposed rats, mucociliary activity was present in areas adjacent to erosions of the turbinates and septum. Abnormal mucus flow patterns, including altered or reversed direction of flow and "whirlpool-like" formation, were observed in all treated rats, but were more severe following chronic exposure. There was a good correlation between the distribution of responses as assessed by histopathology and abnormal mucociliary function at all time points. In conclusion, the mucociliary apparatus continues to function in the nasal passages of rats having localized destruction of nasal epithelium, induced by DMA exposure, and this clearance system responds to alterations of nasal structure by modification of mucus flow patterns.

Age Factors↗
PubMed1975

Interactive mutagenicity of sodium nitrite, dimethylamine, methylurea and ethylurea.

Groups of mice were treated per os with sodium nitrite either alone or in combination with nitrosatable amino compounds and tested in the host mediated assay. When mice were treated with sodium nitrite in combination with dimethylamine a small(4-fold) but significant increase in mutant frequency (MF) was observed. Ethylurea or methylurea in combination with sodium nitrite induced 10- or 850-fold increases in MF, respectively. The response to methylurea was dose-dependent with a 6- and 30-fold increase in MF at 5.4 and 11.5 mg/kg NaNO2 and a 6-fold increase at 108 mg/kg methylurea. That this response reflected gastric nitrosation was shown by the disappearance of the response if NaNO2 administration preceded methylurea treatment by 10 min. High MF's were observed if NaNO2 was administered 10 or 20 min after methylurea.

Animals↗
PubMed1985

Thermal conversion of trimethylamine-N-oxide to trimethylamine and dimethylamine in squids.

The levels of dimethylamine-nitrogen (DMA-N), trimethylamine-nitrogen (TMA-N) and trimethylamine-N-oxide-nitrogen (TMAO-N) were determined in five species of dried squid. Each sample contained extremely high levels of TMAO-N (2558-8064 ppm) and moderate amounts of TMA-N (121-503 ppm) and DMA-N (124-373 ppm). Over 90% of TMAO-N in squid was converted to TMA-N and DMA-N after heating at 200 degrees C for 1 hr; approximately 50% of the volatile TMA-N and DMA-N was lost during the course of the heating. The thermal conversions were accelerated by heat, and possibly involved catalysis by certain tissue constituents. Squids are a popular seafood in most oriental countries, but before appearing on the market they are subjected to a long food-processing procedure. Therefore, a high concentration of TMAO in squids is an important problem, for food technology as well as toxicology.

Animals↗
PubMed1989

Potentiation of ferrous sulphate and ascorbate on the microbial transformation of endogenous trimethylamine N-oxide to trimethylamine and dimethylamine in squid extracts.

The levels of trimethylamine N-oxide (TMAO) in the New Zealand (Nototodarus sloani) species of squid extracts were extremely high (above 9200 ppm). When the extracts were incubated for 2 days at 25 degrees C, approximately 60% TMAO was converted to trimethylamine (TMA) and dimethylamine (DMA). This conversion was very low or negligible at 4 degrees C, but was potentiated by the presence of ferrous sulphate (0.014 M) and ascorbate (0.014 M). Citrobacter freundii and Aeromonas hydrophilia were isolated from the extracts. Cultures of these two micro-organisms and of Escherichia coli were active in catalysing the conversion of TMAO to TMA and DMA either in extract or in aqueous solution. Chloramphenicol (0.416 mg/ml) completely inhibited the growth of these micro-organisms and also effectively blocked the conversion of endogenous TMAO to TMA in the extracts. The present findings suggest that gastro-intestinal flora and dietary ferrous salts and ascorbate may play important roles in the conversion of TMAO to TMA and DMA in man following the ingestion of squid and other TMAO-containing seafoods.

Animals↗
PubMed1985

Endogenous formation of dimethylamine.

An understanding of the biosynthesis and metabolism of dimethylamine (DMA) is important because it is a precursor of dimethylnitrosamine (nitroso-DMA). DMA is the major short-chain aliphatic amine in human and rat urine. DMA is formed from trimethylamine (TMA), which, in turn, is a breakdown product of dietary choline. Enzymes within gut bacteria catalyse both of these reactions; it is not known whether mammalian cells can form DMA. To determine the relative importance of dietary choline, bacteria and other mechanisms for the formation of DMA, we measured DMA excretion in the urine of rats fed on a diet devoid of choline, and in urine of rats with no bacterial colonization of the intestines. We also describe an improved gas-chromatographic method for the measurement of methylamines in biological fluids. In control rats there were significant amounts of DMA within several biological fluids [urine, 54.2 +/- 3.0 mumol/kg body wt. per 24 h (556.2 +/- 37.5 nmol/ml); blood, 18.8 +/- 1.9 nmol/ml; gastric juice, 33.5 +/- 10.5 nmol/ml; means +/- S.E.M.]. Animals eating a diet containing no choline excreted as much MMA and DMA as did choline-supplemented rats (25-35 mumol/kg per 24 h), and they excreted slightly less TMA (2 versus 2.5 mumol/kg per 24 h). Rats with no gut bacteria excreted the same amount of DMA in their urine as did the control animals (45-55 mumol/kg per 24 h). They excreted much less MMA (16.3 +/- 1.5 versus 40.3 +/- 2.6 mumol/kg per 24 h; mean +/- S.E.M.; P less than 0.01), TMA (0.7 +/- 0.2 versus 2.5 +/- 0.5 mumol/kg per 24 h; mean +/- S.E.M.; P less than 0.01) and piperidine (2.0 +/- 0.3 versus 6.3 +/- 0.6 mumol/kg per 24 h; mean +/- S.E.M.; P less than 0.01) in their urine. From our studies we conclude that DMA is present in significant amounts within gastric fluid, an environment that is ideal for nitrosamine formation (under acidic conditions, nitroso-DMA is chemically formed by the reaction of nitrite with DMA). Results also indicate that dietary choline was not the sole precursor for DMA formation and that gut bacteria are not essential for the formation of DMA. Hence in mammals there must be endogenous pathways that are capable of forming DMA; however, these endogenous mechanisms remain unidentified.

Animals↗
PubMed1989

Disposition of 2,4-dichlorophenoxyacetic acid dimethylamine by Fischer 344 rats dosed orally and dermally.

The dimethylamine salt of 14C-ring-labeled 2,4-D was administered to Fischer 344 rats orally (1 and 0.4 mg/kg body weight) and dermally (10 mg/kg body weight). Absorption, distribution, and elimination were determined from 14C-labeled 2,4-D in blood, tissues, and excreta. Quantitatively, most of the orally administered dose (94-96%) became systemically available within 6 h. Following dermal administration 10% of the dose became systemically available over 72 h. However, peak concentrations in blood and kidneys were achieved within 30 min of dosing by either route. By 1.5 h after dosing, 2,4-D concentrations in blood, muscle, liver, and kidneys had decreased in both the orally dosed and dermally dosed animals. Between 2 and 8 h, the blood, muscle, liver and kidney concentrations in dermally dosed animals maintained a plateau while urinary excretion increased, presumably due to continued absorption of 2,4-D from the skin. The concentrations in orally dosed animals continued to decrease. Following 7 h of dermal exposure, skin cleansing removed about 63% of the applied dose; about 17% of the applied dose remained at the site of dermal dosing. At 8 h, 2,4-D concentrations in blood, muscle, liver, and kidneys of dermally dosed animals began to decrease, most likely a result of the removal of the reservoir on the skin. However, 2,4-D continued to be absorbed from skin site, resulting in a slower decline of the 2,4-D concentrations in these tissues over remainder of the 72-h study period. By comparison, in animals that had been orally dosed, the absorbed dose was almost completely excreted within 24 h.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1990

Effects of skin preapplication treatments and postapplication cleansing agents on dermal absorption of 2,4-dichlorophenoxyacetic acid dimethylamine by Fischer 344 rats.

Various methods of preparing dermal application sites in Fischer 344 rats prior to exposure to 2,4-dichlorophenoxyacetic acid dimethylamine salt (2,4-D amine) and the effect of various cleansing agents following exposure were examined by measuring recoveries of 14C-labeled 2,4-D amine in skin, postapplication cleansing solution, blood, and urine. The middorsal area of the rat was the site of application for four treatments tested: (1) hair clipping only, (2) hair clipping followed by an epilatory cream, (3) hair clipping plus shaving with an electrical razor, and (4) as in treatment 3 followed by washing with soap and water. A last preparation was the rat's tail thoroughly brushed with soap and water. The results indicated that the tail retained greater than 75% of the material, thus preventing its absorption into the blood stream and subsequent removal by cleansing. With treatment 1 the dense short hair remaining after clipping impaired the absorption of 2,4-D as evidenced by considerably lower blood and urinary levels than treatments 2-4. With preparations 1-4, 45-61% of the dose was removed with the 7-h postapplication cleansing and a further 5-6% with the subsequent 23-h cleansing. In other studies using preparation 3 above, the following cleansing agents were tested: soap and water, water, isopropanol, acetone, and Rad-Con, a foam-producing cleanser. Rad-Con removed more 2,4-D from the skin than other cleansing agents after 7 h of exposure and more than soap and water after 23 h. The percentages of 2,4-D left on the skin following either 7- or 23-h cleansing with Rad-Con were 8-12%, nearly half those following the other cleansing agents. Cleansing agents other than Rad-Con presented little advantage over soap and water. With all cleansing agents, delaying cleansing from 7 to 23 h after exposure resulted in higher blood and urinary levels of 2,4-D measured 24 h after application.

1-Propanol↗
PubMed1992

Percutaneous penetration of 2,4-dichlorophenoxyacetic acid and 2,4-D dimethylamine salt in human volunteers.

The percutaneous penetration of 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4-D dimethylamine salt (DMA) was evaluated separately in five male volunteers who participated in both experiments. Urine samples collected for 144 h following dermal applications of 10 mg to the dorsum of the hand (9 cm2) were analyzed for 2,4-D. Following the acid application, an average of 4.46 +/- 0.849% was recovered in the urine and a significantly lower amount of 1.76 +/- 0.568% following the DMA application. Significantly higher amounts of 2,4-D DMA (7.68 +/- 0.493 mg) were washed off the hand 6 h following application as compared with 2,4-D acid (5.35 +/- 0.384 mg). These results indicate that, in addition to the differences in physical and chemical properties of the two compounds that will affect absorption, the amount of the chemical absorbed is related inversely to the amount of washed off. Urinary excretion of 2,4-D was not complete in all volunteers 144 h following either application, but in all cases it was approaching the limit of detection. An average of 84.8 +/- 2.55% and 76.8 +/- 8.05% of the total recovered in 144 h was recovered in the urine 96 h following 2,4-D acid and 2,4-D DMA application, respectively. Average, approximated half-lives for excretion were 39.5 +/- 8.1 h for the acid application and 58.5 +/- 13.2 h for the DMA application.

2,4-Dichlorophenoxyacetic Acid↗