Disease relevance of Dimethylethanolamine

• Of a series of inhibitors and protectors, 2-dimethylaminoethanol was the most potent inhibitor of choline uptake and the most potent protector of both hematopoietic progenitor cells and murine L1210 leukemia cells [1].
• Developmental toxicity study in Fischer 344 rats by whole-body exposure to N,N-dimethylethanolamine vapor [2].
• RESULTS: Embryos exposed to 250-750 microM DMAE for 26 hr developed craniofacial hypoplasia and open neural tube defects in the forebrain, midbrain, and hindbrain regions [3].
• The effects of lifetime treatment with dimethylaminoethanol on longevity and cryptogenic neoplasm formation were studied in females of two mouse sub-lines, the C3H/HeN which carries a germinal mammary tumor provirus and the C3H/HeJ(+) which also carries the exogenous mammary tumor virus [4].
• A case of essential tremor since early adultness is presented, which has been treated successfully with the acetylcholine precursor 2-dimethylaminoethanol (deanol) for 10 years [5].

Psychiatry related information on Dimethylethanolamine

• Letter: Dimethylaminoethanol ineffective in Huntington's disease [6].
• Deanol and Tourette syndrome [7].
• Double-blind trial of 2-dimethylaminoethanol in Alzheimer's disease [8].
• Deanol seems to be an ineffective treatment for the normal slowing of cognitive function seen in the normal elderly person or those elderly with only minimal cognitive decline and free of symptoms of dementia [9].
• These observations have both practical and heuristic implications for the management of patients and for further research into the pharmacology of affective disorders and deanol [10].

High impact information on Dimethylethanolamine

• The intravenous administration of dimethylethanolamine in the rat promotes a selective enrichment of liver membranes with polyunsaturated phosphatidylcholines [11].
• DME effectively inhibited only the GmCK2-encoded choline kinase activity [12].
• Deanol in the treatment of levodopa-induced dyskinesias [13].
• This study suggests that H2O2-induced apoptotic cell death is associated with prolonged ERK activation and nuclear translocation in DHA-enriched OLN 93 cells, while both phenomena are prevented by dEa supplements [14].
• The apparent EC50 values (concn. giving half of maximal effect) for cytidylyltransferase translocation were similar for choline and dimethylethanolamine (25 and 27 microM respectively) [15].

Chemical compound and disease context of Dimethylethanolamine

• These findings may explain discrepant results from laboratories seeking increases in brain acetylcholine or clinical improvement in patients with tardive dyskinesia after deanol treatment [16].
• The authors conducted placebo-controlled double-blind studies of physostigmine, choline, and deanol in 12 patients with tardive dyskinesia [17].
• The administration of either deanol, lithium carbonate or placebo added to the neuroleptic treatment did not produce a statistically significant improvement of tardive dyskinesia in our patient population as a whole [18].
• On the basis of its pharmacologic action Deanol (dimethyl aminoethanol) was hypothesized to be of benefit in the Gilles de la Tourette Syndrome [19].
• A role for choline during early stages of mammalian embryogenesis has not been established, although recent studies show that inhibitors of choline uptake and metabolism, 2-dimethylaminoethanol (DMAE), and 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3), produce neural tube defects in mouse embryos grown in vitro [20].

Biological context of Dimethylethanolamine

• Treatment with deanol also caused an increase in the concentration of choline in kidneys, and markedly inhibited the rates of oxidation and phosphorylation of intravenously administered [3H-methyl]choline [21].
• Formation of phosphatidyl-mono- and dimethylethanolamine and that of phosphatidylcholine increased significantly in the morning, reaching maximal values on the afternoon of proestrus; they decreased thereafter during estrus, metestrus, and diestrus [22].
• The effects of deanol on cognitive performance and electrophysiology in elderly humans [9].
• In control rodent brain, liver, heart, lung and plasma, we detected no free endogenous deanol (less than 1 nmol/g) [23].
• The structure-activity relationships of 2-dimethylaminoethanol and its analogues as protectors against mechlorethamine cytotoxicity and as inhibitors of choline uptake were evaluated [1].

Anatomical context of Dimethylethanolamine

• Release of cytidylyltransferase into cytosol was only observed in hepatocytes supplemented with choline or dimethylethanolamine [15].
• Dimethylethanolamine (0.5-1 mM), added to serum-starved NIH 3T3 fibroblasts, stimulated DNA synthesis 11-32-fold, and it also greatly enhanced the relatively modest (15-20-fold) mitogenic effect of insulin [24].
• The data emphasize the need for further investigation into the mode of action of deanol and question its suggested role as an immediate precursor of ACh synthesis in the central nervous system [23].
• Likewise, there was no detectable elevation in ACh levels in rat whole brain, cortex, striatum or hippocampus after a 15-minute pretreatment with 550 mg/kg of deanol (i.p.). The only elevation in ACh levels which we detected occurred selectively in the striatum of mice pretreated with a massive dose (900 mg/kg i.p.) of deanol for 30 minutes [23].
• The antiguanidine agents choline, dimethylethanolamine and tetraethylammonium, but not methionine, inhibited guanidine uptake by HeLa cells [25].

Associations of Dimethylethanolamine with other chemical compounds

• The presence of either N-methylethanolamine (MME) or N,N-dimethylethanolamine (DME) in the growth medium resulted in significant increase of the corresponding phospholipid, phosphatidyl-N-monomethylethanolamine (PMME) or phosphatidyl-N,N-dimethylethanolamine (PDME) [26].
• The synthesis from dimethylaminoethanol and acrylyl chloride was described and the hydration with times in an aqueous medium measured by NMR spectroscopy was presented [27].
• The cells grown in presence of either MME or DME in the culture medium did not show an increased incorporation of methyl groups from AdoMet into the total phospholipids after addition of exogenous acceptors [26].
• It appears that the microsomal enzyme was largely affected by the drug itself because the hydrolysis products of centrophenoxine, viz., N,N-dimethylaminoethanol and p-chlorophenoxyacetic acid, were less inhibitory [28].
• Six tertiary amines which represent commonly used promotors for the formation of PUs from diisocyanates and polyols, namely pentamethyldiethylenetriamine, diazabicyclooctane, N-methylmorpholine, N-ethylmorphine, 1,4-dimethylpiperazine and N,N-dimethylethanolamine, were sorbed onto the new resin [29].

Gene context of Dimethylethanolamine

• This work suggests that MME and DME incorporated into the corresponding phospholipids function as effective substrates for phospholipid-N-methylation [26].
• Conversion of radiolabelled ethanolamine plasmalogen into the dimethylethanolamine and choline analogue via transphosphatidylation by phospholipase D from cabbage [30].
• Modification with monomethylethanolamine was more effective than that with dimethylethanolamine in slowing down the transport of IgG1 and appeared to cause accumulation of IgG1 within the cells [31].
• A potential role for phospholipids in the regulation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase in cultured C-6 glial cells. Effects of N,N-dimethylethanolamine [32].
• Both [18F]CH2BrF and [18F]CH2FOTf were applied to solid-supported [18F]fluoromethylation of N,N-dimethylaminoethanol on a Sep-Pak Plus C18 cartridge to produce the 18F-labeled choline analogue, (beta-hydroxyethyl)dimethyl-[18F]fluoromethylammonium ([18F]fluorocholine) [33].

Analytical, diagnostic and therapeutic context of Dimethylethanolamine

• Deanol was not found to be effective in this group of patients; the authors suggest that this drug should not be assumed to be generally effective unless effectiveness is verified by a large placebo-controlled double-blind study [17].
• Brain uptake of the [11C]choline product was six times greater after HPLC removal of deanol because doses of less than 1 microgram/kg significantly inhibit [14C]choline brain uptake [34].
• Ten hospitalized chronic psychotic patients with symptoms of tardive dyskinesia were given deanol and placebo, each for 8 weeks following a double-bline, crossover design [35].
• However, there was a tendency for a significant increase in the schizophrenic symptoms of the deanol-treated group relative to the control group [36].
• Dimethylaminoethanol (deanol): effect on apomorphine-induced stereotypy and an animal model of tardive dyskinesia [37].

References