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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↗
PubMed1983

Toxicity of nitrite and dimethylamine in rats.

Weanling male Wistar strain rats were administered, through the drinking water, nitrite (0.2%) and dimethylamine (DMA) (0.2%), either singly or in combination for 9 months. Some animals also received 0.5% butylated hydroxytoluene (BHT) in the diet. Nitrite, as well as DMA, caused higher in vitro lipoperoxidation, free lysosomal enzyme activities and cytosolic superoxide dismutase activity in liver. Some of these increases viz., the enzyme activities in liver, were counteracted to a significant extent in the rats receiving a dietary supplement of BHT. The results indicate that nitrite and DMA may induce toxicity through some free radical reactions and that BHT can provide some protection.

Acid Phosphatase↗
PubMed2005

Endotoxin adsorbent using dimethylamine ligands.

Various adsorbents have been investigated for removing endotoxin from protein solutions. It is believed that electrostatic interaction and hydrophobic intermolecular interaction are the main interactions in adsorption of endotoxin. In this work, a series of novel molecular recognition adsorbents for removal of endotoxin with dimethylamine ligand were prepared by coupling ligands on polymethyl methacrylate. We found that its adsorption capacity of endotoxin increased almost 8 times in the presence of a hydroxyl group at beta-site of ligand. The computer simulation showed that the hydroxyl group at beta-site could form H bond with endotoxin, as a result an octatomic ring was formed. The spacer in adsorbent and the long alkyl chain in endotoxin were located at the same side of the octatomic ring. In this situation, electrostatic interaction, H bond, cooperative effect of octatomic ring and hydrophobic intermolecular interaction effected simultaneously. The combination of endotoxin with adsorbent was tight and adsorption capacity was effectually increased.

Adsorption↗
PubMed2004

QSPR/QSAR in N-[(dimethylamine)methyl] benzamides substituents groups influence upon electronic distribution and local anesthetics activity.

It was determined, with a systematic mode, the carbonyl group frequency in the region of the infrared of N-[(dimethylamine)methyl] benzamides 4-substituted (set A) and their hydrochlorides (set B), that had its local anesthetical activity evaluated. The application of the Hammett equation considering the values of the absorption frequency of carbonyl group, nu(C=O,) using the electronic constants sigma, sigma(I), sigma(R), I and R leads to meaningful correlation. The nature and the contribution of substituent group electronic effects on the polarity of the carbonyl group was also analyzed. The use of the nu(C=O) as an experimental electronic parameter for QSPR studies was validated.

Anesthetics, Local↗
PubMed2005

Influence of N-dodecyl-N,N-dimethylamine N-oxide on the activity of sarcoplasmic reticulum Ca(2+)-transporting ATPase reconstituted into diacylphosphatidylcholine vesicles: efects of bilayer physical parameters.

Sarcoplasmic reticulum Ca-transporting ATPase (EC 3.6.1.38) was isolated from rabbit white muscle, purified and reconstituted into vesicles of synthetic diacylphosphatidylcholines with monounsaturated acyl chains using the cholate dilution method. In fluid bilayers at 37 degrees C, the specific activity of ATPase displays a maximum (31.5+/-0.8 IU/mg) for dioleoylphosphatidylcholine (diC18:1PC) and decreases progressively for both shorter and longer acyl chain lengths. Besides the hydrophobic mismatch between protein and lipid bilayer, changes in the bilayer hydration and lateral interactions detected by small angle neutron scattering (SANS) can contribute to this acyl chain length dependence. When reconstituted into dierucoylphosphatidylcholine (diC22:1PC), the zwitterionic surfactant N-dodecyl-N,N-dimethylamine N-oxide (C12NO) stimulates the ATPase activity from 14.2+/-0.6 to 32.5+/-0.8 IU/mg in the range of molar ratios C12NO:diC22:1PC=0/1.2. In dilauroylphosphatidylcholines (diC12:0PC) and diC18:1PC, the effect of C12NO is twofold-the ATPase activity is stimulated at low and inhibited at high C12NO concentrations. In diC18:1PC, it is observed an increase of activity induced by C12NO in the range of molar ratios C12NO:diC18:1PC< or =1.3 in bilayers, where the bilayer thickness estimated by SANS decreases by 0.4+/-0.1 nm. In this range, the 31P-NMR chemical shift anisotropy increases indicating an effect of C12NO on the orientation of the phosphatidylcholine dipole N(+)-P- accompanied by a variation of the local membrane dipole potential. A decrease of the ATPase activity is observed in the range of molar ratios C12NO:diC18:1PC=1.3/2.5, where mixed tubular micelles are detected by SANS in C12NO+diC18:1PC mixtures. It is concluded that besides hydrophobic thickness changes, the changes in dipole potential and curvature frustration of the bilayer could contribute as well to C12NO effects on Ca(2+)-ATPase activity.

Animals↗
PubMed2004

Effects of non-ionic surfactants N-alkyl-N,N-dimethylamine-N-oxides on the structure of a phospholipid bilayer: small-angle X-ray diffraction study.

Effects of non-ionic surfactants N-alkyl-N,N-dimethylamine-N-oxides (C(n)NO, n is the number of alkyl carbons) on the structure of egg yolk phosphatidylcholine (EYPC) bilayers in the lamellar fluid phase was studied by small-angle X-ray diffraction as a function of H(2)O:EYPC and C(n)NO:EYPC molar ratios. The bilayer thickness d(L) and the lipid surface area at the bilayer-aqueous interface S(L) were calculated from the repeat period, d of the lamellar phase, based on the model that water and EYPC + CnNO molecules form separated layers and that their molecular volumes are additive. In the studied range of m=CnNO:EYPC molar ratios up to 1:1, d(L) and S(L) change linearly. The slopes Delta L = delta dL/ delta m and Delta S= delta S L / delta m are equal to -0.876 +/- 0.027 nm and 0.347 +/- 0.006 nm2 for C(6)NO, -1.025+/-0.060 nm and 0.433+/-0.025 nm(2) for C(8)NO, -0.836+/-0.046 nm and 0.405+/-0.018 nm(2) for C(10)NO, -0.604+/-0.015 nm and 0.375+/-0.007 nm(2) for C(12)NO, -0.279+/-0.031 nm and 0.318+/-0.005 nm(2) for C(14)NO, -0.0865+/-0.070 nm and 0.2963 +/-0.014 nm(2) for C(16)NO, and -0.040+/-0.022 nm and 0.297+/- 0.002 nm(2) for C(18)NO, respectively, at full bilayer hydration. The peak-peak distance in the bilayer electron density profile, which relates to the P-P distance d(PP), obtained from the first four diffraction peaks by the Fourier transform also depends linearly on m, and the slope Delta PP = delta dPP/delta m is -0.528+/-0.065 nm for C(6)NO, -0.680+/-0.018 nm for C(8)NO, -0.573+/-0.021 nm for C(10)NO, -0.369+/-0.075 nm for C(12)NO, -0.190+/-0.015 for C(14)NO, -0.088+/-0.016 nm for C(16)NO and -0.094+/-0.016 nm for C(18)NO. The effects of C(n)NO on Delta(L), Delta(S) and Delta(PP) are the results of C(n)NO insertion into EYPC bilayers and depend on the hydrophobic mismatch between C(n)NO and EYPC hydrocarbon chains and on the lateral interactions of C(n)NO and EYPC in the bilayer.

Chemical Phenomena↗
PubMed2006

Accurate quantification of dimethylamine (DMA) in human urine by gas chromatography-mass spectrometry as pentafluorobenzamide derivative: evaluation of the relationship between DMA and its precursor asymmetric dimethylarginine (ADMA) in health and disease.

Dimethylamine [DMA, (CH(3))(2)NH)] is abundantly present in human urine. Main sources of urinary DMA have been reported to include trimethylamine N-oxide, a common food component, and asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthesis. ADMA is excreted in the urine in part unmetabolized and in part after hydrolysis to DMA by dimethylarginine dimethylaminohydrolase (DDAH). Here we describe a GC-MS method for the accurate and rapid quantification of DMA in human urine. The method involves use of (CD(3))(2)NH as internal standard, simultaneous derivatization with pentafluorobenzoyl chloride and extraction in toluene, and selected-ion monitoring of m/z 239 for DMA and m/z 245 for (CD(3))(2)NH in the electron ionization mode. GC-MS analysis of urine samples from 10 healthy volunteers revealed a DMA concentration of 264+/-173 microM equivalent to 10.1+/-1.64 micromol/mmol creatinine. GC-tandem MS analysis of the same urine samples revealed an ADMA concentration of 27.3+/-15.3 microM corresponding to 1.35+/-1.2 micromol/mmol creatinine. In these volunteers, a positive correlation (R=0.83919, P=0.0024) was found between urinary DMA and ADMA, with the DMA/ADMA molar ratio being 10.8+/-6.2. Elevated excretion rates of DMA (52.9+/-18.5 micromol/mmol creatinine) and ADMA (3.85+/-1.65 micromol/mmol creatinine) were found by the method in 49 patients suffering from coronary artery disease, with the DMA/ADMA molar ratio also being elevated (16.8+/-12.8). In 12 patients suffering from end-stage liver disease, excretion rates of DMA (47.8+/-19.7 micromol/mmol creatinine) and ADMA (5.6+/-1.5 micromol/mmol creatinine) were found to be elevated, with the DMA/ADMA molar ratio (9.17+/-4.2) being insignificantly lower (P=0.46). Between urinary DMA and ADMA there was a positive correlation (R=0.6655, P<0.0001) in coronary artery disease, but no correlation (R=0.27339) was found in end-stage liver disease.

Acetazolamide↗
PubMed2005

Genotoxicity of the herbicide 2,4-dichlorophenoxyacetic and a commercial formulation, 2,4-dichlorophenoxyacetic acid dimethylamine salt. I. Evaluation of DNA damage and cytogenetic endpoints in Chinese Hamster ovary (CHO) cells.

Genotoxicity of the 2,4-dichlorophenoxyacetic acid (2,4-D) and a commercially-used derivative, 2,4-D dimethylamine salt (2,4-D DMA), was evaluated in CHO cells using SCE and single cell gel electrophoresis (SCGE) assays. Log-phase cells were treated with 2.0-10.0 microg/ml of herbicides and harvested 24 and 36 h later for SCE analysis. Both agents induced significant dose-dependent increases in SCE, regardless of the harvesting time (2,4-D: r=0.98 and r=0.88, P<0.01, for 24 and 36 h harvesting times; 2,4-D DMA: r=0.97 and r=0.88, P<0.01, for 24 and 36 h harvesting times). Neither test compound altered cell-cycle progression or proliferative replication index (P>0.05), but the higher doses of both compounds reduced the mitotic index of cultures harvested at 24 and 36 h (P<0.05). A 90-min treatment with 2.0-10.0 microg/ml 2,4-D and 2,4-D DMA produced dose-dependent increases in the frequency of DNA-strand breaks detected in the SCGE assay, both in cultures harvested immediately after treatment and in cultures harvested 36 h later. The doses of 2,4-D and 2,4-D DMA were equally genotoxic in all of the assays. The results indicate that 2,4-D induces SCE and DNA damage in mammalian cells, and should be considered as potentially hazardous to humans.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1998

Determination of dimethylamine and other low-molecular-mass amines using capillary electrophoresis with laser-induced fluorescence detection.

The potential of capillary electrophoresis (CE) with laser-induced fluorescence (LIF) detection for the separation and determination of dimethylamine (DMA) and other low-molecular-mass amines involving precolumn derivatization with fluorescein isothiocyanate isomer I (FITC) was investigated. Different variables that affect derivatization (pH, FITC concentration, reaction time and temperature) and separation (buffer concentration, addition of various organic modifiers, applied voltage and length of capillary) were studied. The linearity, reproducibility and reliability of the method were evaluated. The estimated instrumental detection limit for a 2-s pressure injection of the FITC-DMA derivative was 50 pg/ml (10(-9) M), using LIF detection with excitation and emission wavelengths of 488 nm and 520 nm, respectively. However, for practical reasons, a minimum of 5 ng/ml DMA should be subjected to the derivatization. The applicability of the described method to the extract of atmospheric aerosol samples was demonstrated.

Dimethylamines↗
PubMed2005

Derivatization using dimethylamine for tandem mass spectrometric structure analysis of enzymatically and acidically depolymerized methyl cellulose.

Structure analysis of partially depolymerized methyl cellulose was performed by nanoelectrospray ionization tandem mass spectrometry (nano-ESI-MS/MS) and by matrix-assisted laser desorption/ionization tandem mass spectrometry (MALDI-MS/MS). Dimethylamine (DMA) was used for the first time as a reducing end derivatization reagent for oligosaccharides. This is an attractive reagent since it could be easily removed from the reaction mixture. Most important it also introduces a basic functional group that increased the sensitivity in both MALDI and nano-ESI. Depolymerization was made in two ways: one by the cellulose selective endoglucanase 5A from Bacillus agaradhaerens (Ba Cel5A) and the other by trifluoroacetic acid. The DMA derivatives formed both protonated and sodiated molecules in nano-ESI and MALDI. Tandem MS of protonated molecules yielded predominantly Y fragments from which the distribution of the substituents in the oligomers could be measured. Fragments obtained in tandem MS of sodiated molecules provided information regarding the positions of the substituents within the anhydroglucose units (AGUs). It was found that Ba Cel5A could cleave glucosidic bonds also if the AGU on the reducing side of the bond was fully methylated. The combination of DMA derivatization and tandem MS was demonstrated as a tool for the characterization of endoglucanase selectivity.

Cellulase↗
PubMed1994

Inhibition and inactivation of the F1 adenosinetriphosphatase from Bacillus PS3 by dequalinium and activation of the enzyme by lauryl dimethylamine oxide.

The F1-ATPase from Bacillus PS3 (TF1) hydrolyzes 50 microM ATP in three kinetic phases. An initial burst rapidly decelerates to a partially inhibited, intermediate phase, which, in turn, gradually accelerates to an uninhibited, final steady-state rate. Lauryl dimethylamine oxide (LDAO) stimulates the final rate over 4-fold. The stimulatory effect saturates at about 0.1% LDAO. Under these conditions, the intermediate phase is nearly absent. Dequalinium inhibits TF1 reversibly in the dark in the presence or absence of LDAO. The apparent affinity of TF1 for dequalinium increases in the presence of LDAO. Dixon plots of the initial rates of the intermediate phase and the final rates against dequalinium concentration at a series of fixed ATP concentrations in the presence and absence of 0.03% LDAO indicate noncompetitive inhibition in each case. Replots of the slopes of the Dixon plots for the initial rate of the intermediate phase and the final rate against 1/[ATP] reveal apparent Km values of 770 microM and 144 microM, respectively, when obtained in the absence of LDAO. The apparent Km values determined from the data obtained in the presence of LDAO for the same phases are 303 microM and 163 microM, respectively. These results suggest that LDAO stimulates ATPase activity either by increasing the affinity of noncatalytic sites for ATP, which promotes release of inhibitory MgADP from a catalytic site, or by directly promoting release of MgADP from the affected catalytic site. Dequalinium retards this process without affecting the affinity of noncatalytic sites for ATP. When irradiated in the presence of dequalinium, TF1 is rapidly inactivated with an apparent Kd of 12.5 microM in the presence or absence of LDAO.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed2003

N-nitrosodimethylamine formation by free-chlorine-enhanced nitrosation of dimethylamine.

The formation of N-nitrosodimethylamine (NDMA) by the nitrosation of dimethylamine (DMA) is greatly enhanced by the presence of free chlorine (HOCl). The effect of HOCl appears at first to be contrary because HOCl rapidly oxidizes nitrite and hence should reduce NDMA formation from a mechanism involving classical nitrosation. The enhanced nitrosation by the presence of HOCl is, however, consistent with a mechanism that involves the formation of a highly reactive nitrosating intermediate such as dinitrogen tetroxide (N2O4) formed during the oxidation of nitrite to nitrate. This mechanism is quite unlike another recently proposed NDMA formation pathway involving the rate-limiting oxidation of DMA directly by monochloramine. NDMA formation by the proposed HOCl-enhanced nitrosation pathway is inhibited by the presence of ammonia and occurs very quickly, only during the short period during which nitrite oxidation occurs. The general importance of this NDMA formation mechanism in actual drinking water appears to be limited by the amount of DMA and nitrite typically present. The mechanism described here, however, suggests the potential involvement of other nitrogen redox reactions that may produce reactive intermediates leading to the indirect and incidental formation of NDMA in the presence of appropriate organic nitrogen precursor.

Chlorine↗
PubMed2005

UV photolytic mechanism of N-nitrosodimethylamine in water: dual pathways to methylamine versus dimethylamine.

The direct ultraviolet (UV) photolysis of N-nitrosodimethyl-amine (NDMA), a well-known potential carcinogen, was investigated in aqueous solution with its degradation products analyzed quantitatively. NDMA is known to be photolyzed either to dimethylamine (DMA) or to methylamine (MA) by two distinct pathways. However, the mechanism through which NDMA is photolyzed to DMA is still not clearly understood. This study reveals a new mechanistic pathway of NDMA photolysis to DMA by identifying the factors influencing the photolysis pathway. The two pathways of NDMA photolysis were found to be strongly dependent on the initial NDMA concentration and solution pH. Increasing the initial NDMA concentration clearly favored the DMA formation path. DMA production was optimized in the region of pH 4-5. The nitrite ion (NO2-) produced from the NDMA photolysis was identified as a key reagent in directing the NDMA photolysis toward DMA production. The observed photolytic behaviors of NDMA photolysis could be successfully explained in terms of the new mechanism involving the role of NO2-.

Chromatography, High Pressure Liquid↗
PubMed2005

Femtosecond dynamics after ionization: 2-phenylethyl-N,N-dimethylamine as a model system for nonresonant downhill charge transfer in peptides.

The cation of 2-phenylethyl-N,N-dimethylamine (PENNA) offers two local sites for the charge: the amine group and 0.7 eV higher in energy the phenyl chromophore. In this paper, we investigate the dynamics of the charge transfer (CT) from the phenyl to the amine site. We present a femtosecond resonant two-color photoionization spectrum which shows that the femtosecond pump laser pulse is resonant in the phenyl chromophore. As shown previously with resonant wavelengths the aromatic phenyl chromophore can be then selectively ionized. Because the state "charge in the phenyl chromophore" is the first excited state in the PENNA cation, it can relax to the lower-energetic state "charge in the amine site". To follow this CT dynamics, femtosecond probe photoabsorption of green light (vis) is used. The vis light is absorbed by the charged phenyl chromophore, but not by the neutral phenyl and the neutral or cationic amine group. Thus, the absorption of vis photons of the probe laser pulse is switched off by the CT process. For detection of the resonant absorption of two or more vis photons in the cation the intensity of a fragmentation channel is monitored which opens only at high internal energy. The CT dynamics in PENNA cations has a time constant of 80 +/- 28 fs and is therefore not a purely electronic process. Because of its structural similarity to phenylalanine, PENNA is a model system for a downhill charge transfer in peptide cations.

Dimethylamines↗
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↗
PubMed1981

Possible formation of nitrosamine in guinea pigs following exposure to nitrogen dioxide and dimethylamine.

The possibility of formation of nitrosamine was investigated in animals exposed to a combination of dimethylamine (DMA) and NO2. First, the distribution and covalent binding of DMA and dimethylnitrosamine (DMN) in rats and guinea pigs were determined. The apparent volume of distribution and biological half-life for [14C]-DMA or [14C]DMN did not reveal any species difference. In general, there were no marked differences in accumulation of radioactivity in tissues of guinea pigs and rats 4 h after the administration of DMA, while the guinea pig tissues showed higher accumulation after DMN administration. Nucleic acid fractions prepared from liver and lungs of both species following administration of DMN or DMA in vivo showed much higher covalent binding with DMN than with DMA. Furthermore, the covalent binding of DMN was found to be due to bioactivation, whereas the DMA binding was nonspecific. Since guinea pig liver showed a higher degree of covalent binding than rat liver, this species was used to investigate the possible increase in covalent binding in the presence of NO2 and DMA as a reflection of DMN formation. There was no evidence of enhancement of covalent binding when animals pretreated with [14C]-DMA were exposed for various lengths of time to different concentrations of NO2.

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↗