2-dimethylaminoethanol appears as a clear colorless liquid with a fishlike odor. Flash point 105°F. Less dense than water. Vapors heavier than air. Toxic oxides of nitrogen produced during combustion. Used to make other chemicals.
颜色/状态：
Colorless liquid
气味：
Amine odor
闪点：
38 °C c.c.
溶解度：
greater than or equal to 100 mg/mL at 73° F (NTP, 1992)
蒸汽密度：
3.03 (NTP, 1992) (Relative to Air)
蒸汽压力：
3.18 mm Hg at 25 °C
亨利常数：
Henry's Law constant = 1.8X10-9 atm-cu m/mol at 25 °C (est)
In male Wistar rats, DMAE was oxidized rapidly to the N-oxide of DMAE, representing the primary urinary metabolite. However, only 13.5 % of the administered dose was eliminated by the 24 hour time point, suggesting that most of the DMAE was routed toward phospholipid biosynthetic pathways. In humans, 33% of an injected 1 g (10 mmol) dose of DMAE was excreted unchanged. It was suggested that the remaining dose might have been demethylated to ethanolamine directed toward normal metabolic pathways.[NTP; Dimethylethanolamine (DMAE)
Specific methods utilizing combined gas chromatography mass spectrometry were used to measure the metabolism of [(2)H6]deanol and its effects on acetylcholine concentration in vitro and in vivo. In vitro [(2)H6]deanol was rapidly taken up by rat brain synaptosomes, but was neither methylated nor acetylated. [(2)H6]Deanol was a weak competitive inhibitor of the high affinity transport of [(2)H4]choline, thus reducing the synthesis of [(2)H4]acetylcholine. In vivo [(2)H6]deanol was present in the brain after i.p. or p.o. administration, but was not methylated or acetylated. Treatment of rats with [(2)H6]deanol significantly increased the concentration of choline in the plasma and brain but did not alter the concentration of acetylcholine in the brain. Treatment of rats with atropine (to stimulate acetylcholine turnover) or with hemicholinium-3 (to inhibit the high affinity transport of choline) did not reveal any effect of [(2)H6]deanol on acetylcholine synthesis in vivo. However, since [(2)H6]deanol did increase brain choline, it may prove therapeutically useful when the production of choline is reduced or when the utilization of choline for the synthesis of acetylcholine is impaired.
Choline (N,N,N-trimethylethanolamine), which is widely distributed in membrane lipids and is a component of sediment biota, has been shown to be utilized anaerobically by mixed prokaryote cultures to produce methane but not by pure cultures of methanogens. Here, we show that five recently isolated Methanococcoides strains from a range of sediments (Aarhus Bay, Denmark; Severn Estuary mudflats at Portishead, United Kingdom; Darwin Mud Volcano, Gulf of Cadiz; Napoli mud volcano, eastern Mediterranean) can directly utilize choline for methanogenesis producing ethanolamine, which is not further metabolized. Di- and monomethylethanolamine are metabolic intermediates that temporarily accumulate. Consistent with this, dimethylethanolamine was shown to be another new growth substrate, but monomethylethanolamine was not. The specific methanogen inhibitor 2-bromoethanesulfonate (BES) inhibited methane production from choline. When choline and trimethylamine are provided together, diauxic growth occurs, with trimethylamine being utilized first, and then after a lag (about 7 days) choline is metabolized. Three type strains of Methanococcoides (M. methylutens, M. burtonii, and M. alaskense), in contrast, did not utilize choline. However, two of them (M. methylutens and M. burtonii) did metabolize dimethylethanolamine. These results extend the known substrates that can be directly utilized by some methanogens, giving them the advantage that they would not be reliant on bacterial syntrophs for their substrate supply.
IDENTIFICATION AND USE: 2-Dimethylaminoethanol (DMAE) is a colorless liquid. DMAE has been used as an ingredient in skin care, and in cognitive function- and mood-enhancing products. Deaner(DMAE p-acetamidobenzoate) was a U.S. prescription drug for more than 20 years until 1983 when it was withdrawn from the market. It was used to treat children with learning and behavior problems. A large number of dietary supplements contain DMAE. The predominant form, when specified, is DMAE bitartrate. DMAE has applications in the chemical and pharmaceutical industries. HUMAN EXPOSURE AND TOXICITY: Severe respiratory symptoms were observed in a single painter exposed to spray paint containing DMAE. Wheal and flare responses occurred after exposure of human volunteers to DMAE but it was interpreted as an irritant. DMAE tartrate administered orally to humans produced mild mental stimulation. At 20 mg/day, there was a gradual increase in muscle tone and perhaps an increased frequency of convulsions in susceptible individuals. Larger doses produced insomnia, muscle tenseness, and spontaneous muscle twitches. Serious cholinergic side effects were reported in a 37-yr-old woman with tardive dyskinesia who had been taking deanol. However, a single 2500 mg dose taken in a suicide attempt had no adverse effects. ANIMAL STUDIES: Acute clinical signs of rat exposure to DMAE vapor included nasal and ocular irritation, respiratory distress, and body weight loss. In the 13-week study, rats were exposed to 0, 8, 24, or 76 ppm DMAE for 6 hr/day, 5 days/week for 13 weeks. The principal exposure-related changes were transient corneal opacity in the 24 and 76 ppm groups; decreased body weight gain for the 76 ppm group; and histopathological lesions of the respiratory and olfactory epithelium of the anterior nasal cavity of the 76 ppm group and of the eye of several 76 ppm group females. DMAE did not induce any neoplasms in mice. In a developmental study in rats there were no effects of DMAE treatment on any gestational parameters, including pre- and post-implantation loss or sex ratio. Fetal body weights per litter were statistically significantly increased at 100 ppm relative to controls. There were no increases in the incidences of total malformations by category (external, visceral or skeletal) or individually. The incidence of six skeletal variations out of 120 noted differed in exposed groups relative to that of control. Four of these variations were decreases in incidence; only one fetal variation, the split (bipartite) cervical centrum, was elevated at 100 ppm relative to controls. DMAE was not genotoxic using the Salmonella/microsome reverse gene mutation test, the CHO/HGPRT forward gene mutation test, a sister chromatid exchange test in cultured CHO cells, and an in vivo peripheral blood micronucleus test in mice.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
对人类无致癌性（未列入国际癌症研究机构IARC清单）。
No indication of carcinogenicity to humans (not listed by IARC).
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
该物质可以通过吸入其蒸汽、通过皮肤接触以及摄入进入人体。
The substance can be absorbed into the body by inhalation of its vapour, through the skin and by ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
毒理性
吸入症状
咳嗽。喉咙痛。灼热感。呼吸困难。症状可能会延迟出现。
Cough. Sore throat. Burning sensation. Laboured breathing. Symptoms may be delayed.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
毒理性
皮肤症状
红肿。疼痛。皮肤烧伤。
Redness. Pain. Skin burns.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
Daily oral exposures (deanol acetamidobenzoate, DMAE, or Deaner) of chinchilla rabbits or humans produced measurable plasma and cerebrospinal concentrations of the parent compound. The drugs were cleared from the plasma by 36 hours post-treatment.[NTP; Dimethylethanolamine (DMAE)
Specific methods utilizing combined gas chromatography mass spectrometry were used to measure the metabolism of [(2)H6]deanol and its effects on acetylcholine concentration in vitro and in vivo. In vitro [(2)H6]deanol was rapidly taken up by rat brain synaptosomes, but was neither methylated nor acetylated. [(2)H6]Deanol was a weak competitive inhibitor of the high affinity transport of [(2)H4]choline, thus reducing the synthesis of [(2)H4]acetylcholine. In vivo [(2)H6]deanol was present in the brain after i.p. or p.o. administration, but was not methylated or acetylated. Treatment of rats with [(2)H6]deanol significantly increased the concentration of choline in the plasma and brain but did not alter the concentration of acetylcholine in the brain. Treatment of rats with atropine (to stimulate acetylcholine turnover) or with hemicholinium-3 (to inhibit the high affinity transport of choline) did not reveal any effect of [(2)H6]deanol on acetylcholine synthesis in vivo. However, since [(2)H6]deanol did increase brain choline, it may prove therapeutically useful when the production of choline is reduced or when the utilization of choline for the synthesis of acetylcholine is impaired.
DMAE is absorbed and rapidly transported to the liver where much of it is metabolized. Approximately 280 nmol (25.2 ug) DMAE/gram plasma was observed in male mice about ten minutes after receiving 300 mg (3.30 mmol) DMAE/kg, intraperitoneally. Approximately 2.41, 1.30, and 0.20% of an administered dose of 30 mg/kg (0.13 mmol/kg) (with 100 u Ci) of (14)Cyprodenate was found in the liver, brain, and plasma, respectively, five minutes after intravenous dosing in male rats.[NTP; Dimethylethanolamine (DMAE)
