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1. Diethanolamine Acetate
2. Diethanolamine Bisulfate
3. Diethanolamine Fumarate
4. Diethanolamine Hydrochloride
5. Diethanolamine Maleate
6. Diethanolamine Maleate (1:1)
7. Diethanolamine Phosphate
8. Diethanolamine Sulfate (1:1)
9. Diethanolamine Sulfate (2:1)
10. Diethanolamine Sulfite
11. Diethanolamine Sulfite (1:1)
12. Diethanolammonium Sulfate
1. 111-42-2
2. 2,2'-iminodiethanol
3. Diolamine
4. Iminodiethanol
5. Bis(2-hydroxyethyl)amine
6. 2-(2-hydroxyethylamino)ethanol
7. 2,2'-dihydroxydiethylamine
8. Diethylolamine
9. Ethanol, 2,2'-iminobis-
10. N,n-diethanolamine
11. Diethanolamin
12. 2,2'-iminobisethanol
13. 2,2'-azanediyldiethanol
14. Di(2-hydroxyethyl)amine
15. N,n'-iminodiethanol
16. Niax Deoa-lf
17. Bis(hydroxyethyl)amine
18. Diaethanolamin
19. Dabco Deoa-lf
20. N,n-bis(2-hydroxyethyl)amine
21. 2,2'-iminodi-1-ethanol
22. N,n-di(hydroxyethyl)amine
23. 2-[(2-hydroxyethyl)amino]ethan-1-ol
24. Nci-c55174
25. H2dea
26. Diolamine [inn]
27. Di(beta-hydroxyethyl)amine
28. 2,2'iminobisethanol
29. Mfcd00002843
30. Bis-2-hydroxyethylamine
31. 61791-44-4
32. Diethylamine, 2,2'-dihydroxy-
33. Poe (2) Tallow Amine
34. 2,2'-iminobis[ethanol]
35. 2-[(2-hydroxyethyl)amino]ethanol
36. Ethanol, 2,2'-iminodi-
37. Nsc 4959
38. Tegoamin Deoa 85
39. Diethanolamine (nf)
40. Diethanolamine [nf]
41. Dihydroxyethyl Tallowamine Oxide
42. Nsc-4959
43. Aze05tdv2v
44. Bis-(2-hydroxy-ethyl)-amine
45. 61791-46-6
46. Chebi:28123
47. Bis(2-hydroxyethyl)tallow Amine Oxide
48. Bis-(2-hydroxyethyl)-tallowamine Oxide
49. Dsstox_cid_1932
50. Dsstox_rid_76411
51. Diolamine (van)
52. Dsstox_gsid_21932
53. Amine,diethyl,2,2'-dihydroxy Diethanolamine
54. Diethanolamin [czech]
55. Diaethanolamin [german]
56. Cas-111-42-2
57. Ccris 5906
58. Hsdb 924
59. Einecs 203-868-0
60. Unii-aze05tdv2v
61. Brn 0605315
62. Diethanolarnine
63. Diethanol Amine
64. Aliphatic Amine
65. Ai3-15335
66. 2,2'-iminobis
67. Diethanolamine, 99%
68. Ethanol,2'-iminodi-
69. N, N-diethanol Amine
70. Ethanol,2'-iminobis-
71. 2, 2'-iminodiethanol
72. Amines, Tallow Alkyl Dihydroxyethyl, Oxides
73. Bis-(2-hydroxyethyl)amine
74. Bmse000371
75. Diolamine [mart.]
76. Diethanol, 2,2'-imino-
77. Diethanolamine [ii]
78. Diethanolamine [mi]
79. Ec 203-868-0
80. Diethylamine,2'-dihydroxy-
81. Schembl2324
82. Bis-(2-hydroxyethyl)-amine
83. Nciopen2_008991
84. Wln: Q2m2q
85. (hoch2 Ch2)2nh
86. Diethanolamine [hsdb]
87. Diethanolamine [iarc]
88. Diethanolamine [inci]
89. Ghl.pd_mitscher_leg0.542
90. 4-04-00-01514 (beilstein Handbook Reference)
91. Bis-(2-hydroxy-ethyl) Amine
92. Ethanol, 2,2'-iminobis-, N-tallow Alkyl Derivs.
93. Mls001065608
94. Bidd:gt0277
95. Diethanolamine [vandf]
96. Bis(2-hydroxyethyl)tallowamine
97. Diethanolamine, Lr, >=98%
98. Chembl119604
99. Schembl5200828
100. Diethanolamine [usp-rs]
101. Dtxsid3021932
102. 2-(2-hydroxy-ethylamino)ethanol
103. 2-(2-hydroxyethylamino)-ethanol
104. Diethanolamine, Biochemical Grade
105. Nsc4959
106. 2,2'-azanediylbis(ethan-1-ol)
107. Diethanolamine, Acs Reagent Grade
108. 2-(2-hydroxy-ethylamino)-ethanol
109. Diethanolamine, Analytical Standard
110. Diethanolamine, Puriss., 99.0%
111. Hms2269d18
112. Str03965
113. Zinc5975487
114. Tox21_201701
115. Tox21_300034
116. Diethanolamine, Bioxtra, >=98.5%
117. Stl264122
118. Akos000119884
119. Tallow Bis-(2-hydroxyethyl)amine Oxide
120. Diethanolamine Reagent Grade 1kg
121. Diethanolamine, Acs Reagent, >=98.5%
122. Ncgc00091478-01
123. Ncgc00091478-02
124. Ncgc00091478-03
125. Ncgc00091478-04
126. Ncgc00254061-01
127. Ncgc00259250-01
128. Diethanolamine, Reagent Grade, >=98.0%
129. Smr000112130
130. Trolamine Impurity B [ep Impurity]
131. Diethanolamine, Bioultra, >=99.5% (gc)
132. Diethanolamine, Saj First Grade, >=98.0%
133. Ft-0624757
134. I0008
135. S0376
136. Diethanolamine, Jis Special Grade, >=99.0%
137. C06772
138. D02337
139. D92250
140. Diethanolamine 1000 Microg/ml In Acetonitrile
141. 2,2'-iminobisethanol, N-tallow Alkyl, N-oxide
142. Q418437
143. Ethanol, 2,2'-iminobis-, N-tallow Alkyl, N-oxide
144. J-506841
145. F2190-0311
146. Z966690660
147. Bfc20619-2edf-4764-8e91-830aa892bd39
148. Ethanol, 2,2'-iminobis-, N-tallow Alkyl Derivs, N-oxides
149. Diethanolamine, Puriss. P.a., Acs Reagent, >=99.0% (gc)
150. Diethanolamine, United States Pharmacopeia (usp) Reference Standard
151. Trolamine Impurity B, European Pharmacopoeia (ep) Reference Standard
152. Diethanolamine, Pharmaceutical Secondary Standard; Certified Reference Material
| Molecular Weight | 105.14 g/mol |
|---|---|
| Molecular Formula | C4H11NO2 |
| XLogP3 | -1.4 |
| Hydrogen Bond Donor Count | 3 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 4 |
| Exact Mass | 105.078978594 g/mol |
| Monoisotopic Mass | 105.078978594 g/mol |
| Topological Polar Surface Area | 52.5 Ų |
| Heavy Atom Count | 7 |
| Formal Charge | 0 |
| Complexity | 28.9 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
The estimated fatal dose of diethanolamine in humans is 20 g.
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 406
(14)C-Diethanolamine (7 mg/kg bw) was given orally to male Fischer 344 rats once or by daily repeat dosing for up to eight weeks. Single oral doses (0.7-200 mg/kg bw) were well absorbed but excreted very slowly. About 20-30% of oral and intravenous doses (7 mg/kg bw) was found in urine (mainly as unchanged diethanolamine), with less than 3% in feces and only 0.2% or less was exhaled (CO2) within 48 h. Most of the diethanolamine was retained in tissues at high concentrations. The tissue-to-blood ratios were 150-200 for the liver and kidney, 30-40 for the lung and spleen and 10-20 for the heart, brain and muscle. Tissue radioactivity was found mainly in aqueous extracts (up to 90%) and 5-10% was organic-extractable.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V77 364 (2000)
(14)C-Diethanolamine was applied to 19.5 sq cm of the dorsal skin (20 mg/sq cm, 1500 mg/kg bw) and covered for 48 hr (no washing) or for 6 hr before it was removed by washing. Absorbed (14)C-diethanolamine was determined in 48-hr urine and feces and from sampled tissues. Unwashed rats absorbed 1.4% and washed animals 0.64% of the dose, while the majority of (14)C-diethanolamine was recovered in the occlusive wrappings (80%) and in skin of the dose site (3.6%). The radioactivity was found in carcass, liver or kidneys but very little in urine (0.11%), feces or blood
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V77 363 (2000)
Studies of the penetration of (14)C-diethanolamine from cosmetic formulations (shampoos hair dyes and body lotions) through human skin samples indicated that approximately 0.1% of the applied dose of shampoo and hair dye formulations was absorbed into the receptor fluid after 5-30 minutes; in a 72-hour repeated dose study with a body lotion formulation, nearly 30% of applied diethanolamine accumulated in the skin and approximately 1% was absorbed into the receptor fluid.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V101 128 (2012)
Dermal absorption of diethanolamine is suggested to occur in rats since N-nitrosodiethanolamine was excreted in the urine of male Sprague-Dawley rats which had been administered diethanolamine by dermal application and given nitrite in their drinking water.
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 403
Treatment of Wistar or Sherman rats with diethanolamine caused increases in the formation of hepatic phospholipids. In addition, dietary administration led to incorporation of ethanolamine into hepatic phospholipids, and repeated oral administration of diethanolamine in drinking water (one to three wk) at a dose of 320 mg/kg/day was found to reduce the level of incorporation of ethanolamine and choline into hepatic and renal phospholipids in Sprague-Dawley rats.
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 403
Dermal absorption of diethanolamine is suggested to occur in rats since N-nitrosodiethanolamine was excreted in the urine of male Sprague-Dawley rats which had been administered diethanolamine by dermal application and given nitrite in their drinking water.
Snyder, R. (ed.). Ethel Browning's Toxicity and Metabolism of Industrial Solvents. 2nd ed. Volume II: Nitrogen and Phosphorus Solvents. Amsterdam-New York-Oxford: Elsevier, 1990., p. 403
Diethanolamine is known to be incorporated into membrane phospholipids. It can be O-phosphorylated and N-methylated to metabolites that are incorporated into polar head groups as aberrant membrane phospholipids (phosphoglyceride and sphingomyelin analogues) via the ethanolamine metabolic pathway.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V101 129 (2012)
After a single intravenous or oral administration of diethanolamine, rats predomnantly excreted the parent compound in the urine; after repeated oral administration, the parent compound was still the major product excreted in the urine but N-methylated metabolites were also detected. The parent compound also accounted for the majority of radioactivity extracted from the liver and brain of rats administered (14)C-diethanolamine; two minor metabolites identified in tissues were N-methyldiethanolamine and N,N-dimethyldiethanolamine.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V101 129 (2012)
Diethanolamine (DEA) is a widely used ingredient in many consumer products and in a number of industrial applications. It has been previously reported that dermal administration of DEA to mice diminished hepatic stores of choline and altered brain development in the fetus. The aim of this study was to use mouse neural precursor cells in vitro to assess the mechanism underlying the effects of DEA. Cells exposed to DEA treatment (3mM) proliferated less (by 5-bromo-2-deoxyuridine incorporation) at 48 hr (24% of control [CT]), and had increased apoptosis at 72 hr (308% of CT). Uptake of choline into cells was reduced by DEA treatment (to 52% of CT), resulting in diminished intracellular concentrations of choline and phosphocholine (55 and 12% of CT, respectively). When choline concentration in the growth medium was increased threefold (to 210 uM), the effects of DEA exposure on cell proliferation and apoptosis were prevented, however, intracellular phosphocholine concentrations remained low. In choline kinase assays, we observed that DEA can be phosphorylated to phospho-DEA at the expense of choline. Thus, the effects of DEA are likely mediated by inhibition of choline transport into neural precursor cells and by altered metabolism of choline. /This/ study/ suggests that prenatal exposure to DEA may have a detrimental effect on brain development.
PMID:17204582 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430108 Niculescu MD et al; Toxicol Sci. 96(2):321-6 (2007).
Diethanolamine increased the incidence and multiplicity of liver tumors in the mouse following chronic exposure. Diethanolamine is known to inhibit cellular choline uptake. Since choline deficiency produces tumors in rodents, diethanolamine, through choline depletion, may result in tumor development in rodents. The potential for diethanolamine to function through this mode of action in humans is not known. The present studies examined the effect of diethanolamine (0-500 mug/mL) and choline depletion on DNA synthesis and changes in expression of genes involved in cell growth pathways in primary cultures of mouse, rat, and human hepatocytes. In mouse and rat hepatocytes DNA synthesis was increased following treatment with 10 mug/mL diethanolamine and higher (3- to 4-fold over control). In contrast, diethanolamine failed to increase DNA synthesis in human hepatocytes. Incubation of hepatocytes in medium containing reduced choline (1/10 to 1/100 of normal medium; 0.898 to 0.0898 mg/L vs. 8.98 mg/L) increased DNA synthesis (1.6- and 1.8-fold of control in mouse and rat hepatocytes, respectively); however, choline depletion did not induce DNA synthesis in human hepatocytes. Mouse and rat hepatocytes incubated in medium supplemented with 2- to 50-fold excess choline reduced diethanolamine-induced DNA synthesis to control levels or below. Gene expression analysis of mouse and rat hepatocytes following diethanolamine treatment showed increases in genes associated with cell growth and decreases in expression of genes involved in apoptotic pathways. These results support the hypothesis that choline depletion is central to the mode of action for the induction of rodent hepatic neoplasia by diethanolamine. Furthermore, since diethanolamine treatment or choline depletion failed to induce DNA synthesis in human hepatocytes, these results suggest that humans may not be at risk from the carcinogenic effects of diethanolamine.
PMID:16014740 Kamendulis LM et al; Toxicol Sci 87 (2): 328-36 (2005)
Diethanolamine which interferes with phospholipid metab produced a loss of mitochondrial integrity after subacute admin to Sprague-Dawley rats.
PMID:442087 Barbee SJ, Hartung R; Toxicol Appl Pharmacol 47 (3): 431-40 (1979)
Diethanolamine inhibited in vitro synthesis of phosphatidyl choline and phosphatidyl ethanolamine in rat liver tissue.
PMID:442086 Barbee SJ, Hartung R; Toxicol Appl Pharmacol 47 (3): 431-40 (1979)
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