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1. Aminomethane
2. Methylamine Bisulfite
3. Methylamine Hydride
4. Methylamine Hydrobromide
5. Methylamine Hydrochloride
6. Methylamine Hydrochloride, 14c-labeled
7. Methylamine Hydrofluoride
8. Methylamine Hydrogen Cyanide
9. Methylamine Hydroiodide
10. Methylamine Ion (1-)
11. Methylamine Nitrate
12. Methylamine Perchlorate
13. Methylamine Sulfate (1:1)
14. Methylamine Sulfate (2:1)
15. Methylamine, 13c-labeled
16. Methylamine, 14c-labeled
17. Methylamine, 15n-labeled
18. Methylamine, Cesium Salt
19. Methylamine, Monopotassium Salt
20. Methylamine, Monosodium Salt
21. Methylammonium
22. Methylammonium Ion
23. Monomethylamine
24. Monomethylammonium Ion
1. Methanamine
2. Aminomethane
3. 74-89-5
4. Monomethylamine
5. Carbinamine
6. Mercurialin
7. N-methylamine
8. Methylaminen
9. Metilamine
10. Metyloamina
11. Methylamine Aq
12. Anhydrous Methylamine
13. Monomethyl Amine
14. Methylamine Solutions
15. Methyl-amine
16. Menh2
17. Ch3nh2
18. Bsf23sj79e
19. Chebi:16830
20. Mfcd00008104
21. Nme
22. Methylaminen [dutch]
23. Metilamine [italian]
24. Metyloamina [polish]
25. Methylamin
26. Methyl Amine
27. Ccris 2508
28. Hsdb 810
29. Methylamine, Anhydrous
30. Einecs 200-820-0
31. Un1061
32. Un1235
33. Unii-bsf23sj79e
34. Ai3-15637-x
35. Methaneamine
36. Methlamine
37. Methlyamine
38. Methyamine
39. Methylammonia
40. Methylarnine
41. Metylamine
42. Methyl Group
43. Methylamine-
44. Mono-methylamine
45. N-methyl Amine
46. Methylamine, In Aqueous Solution
47. Mono Methyl Amine
48. Mono-methyl Amine
49. Methylamine Solution
50. Methylamine Anhydrous
51. Methylamine Solution (42% Or Less)
52. Aminomethylidyneradical
53. H2nme
54. Nh2me
55. Methylamine [mi]
56. Dea Code 8520
57. Methylamine [hsdb]
58. H2nch3
59. Nh2ch3
60. Ec 200-820-0
61. Methylamine Aqueous Solution
62. Methylamine, >=99.0%
63. Methylamine, 2m In Methanol
64. Ch3-nh2
65. Methylamine, Aqueous Solution
66. Integrase Inhibitor, R3{3}
67. Un 1235 (salt/mix)
68. Chembl43280
69. Methylamine, 33% In Ethanol
70. Methylamine, Purum, >99.5%
71. Dtxsid7025683
72. Methylamine, Solution In Ethanol
73. Methylamine, Anhydrous, >=98%
74. Methylamine, Purum, >=99.0%
75. Methanamine-d2;methyl(2h2)amine
76. Methylamine, Ca. 2 M In Ethanol
77. Methyl Of Gamma-n-methylasparagine
78. Methylamine, 2m In Tetrahydrofuran
79. Bcp31897
80. Str00032
81. Bdbm50416492
82. Bp-11399b
83. Stl281863
84. Methylamine Solution, 2.0 M In Thf
85. Akos009031510
86. Db01828
87. Methylamine (ca. 9% In Acetonitrile)
88. Un 1061
89. Methylamine Solution, 2.0 M In Methanol
90. Methylamine Solution, 40 Wt. % In H2o
91. Ft-0628859
92. M0137
93. M1016
94. M2108
95. M2323
96. M2324
97. M3340
98. M3341
99. C00218
100. Q409304
101. Gadodiamide Hydrate Impurity C [ep Impurity]
102. Methylamine Solution, 33 Wt. % In Absolute Ethanol
103. Methylamine, Anhydrous [un1061] [flammable Gas]
104. Methylamine (ca. 7% In N,n-dimethylformamide, Ca. 2.0mol/l)
105. Methylamine, Aqueous Solution [un1235] [flammable Liquid]
106. Polystyrene Am-nh2, Macrobeads, Extent Of Labeling: 0.8-1.4 Mmol/g N Loading
107. 3p8
108. Jandajel(tm)-nh2, 100-200 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 2 % Cross-linked
109. Jandajel(tm)-nh2, 200-400 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 2 % Cross-linked
110. Jandajel(tm)-nh2, 50-100 Mesh, Extent Of Labeling: 1.0 Mmol/g N Loading, 2 % Cross-linked
| Molecular Weight | 31.057 g/mol |
|---|---|
| Molecular Formula | CH5N |
| XLogP3 | -0.7 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Exact Mass | g/mol |
| Monoisotopic Mass | g/mol |
| Topological Polar Surface Area | 26 |
| Heavy Atom Count | 2 |
| Formal Charge | 0 |
| Complexity | 2 |
| 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 |
Methylamine can be converted by semicarbazide-sensitive amine oxidase (SSAO) to formaldehyde and hydrogen peroxide, which have been proven to be toxic towards cultured endothelial cells. /The authors/ investigated whether or not these deaminated products from methylamine can exert potentially hazardous toxic effects in vivo. Long lasting residual radioactivity in different tissues was detected following administration of [14C]-methylamine in the mouse. Approximately 10% of the total administered radioactivity could even be detected 5 days after injection of [14C]-methylamine. Eighty percent of the formation of irreversible adducts can be blocked by a highly selective SSAO inhibitor, (E)-2-(4-fluorophenethyl)-3-fluoroallylamine hydrochloride (MDL-72974A). The residual radioactivity was primarily associated with the insoluble tissue components and the soluble macromolecules. Radioactively labelled macromolecules were fragmented following enzymatic proteolysis. Results suggest that the formaldehyde derived from methylamine interacts with proteins in vivo. In the streptozotocin-induced diabetic mice, both SSAO activity and the formation of residual radioactivity were found to be significantly increased in the kidney. Chronic administration of methylamine enhances blood prorenin level, which strongly suggests that uncontrolled deamination of methylamine may be a risk factor for initiation of endothelial injury, and subsequent genesis of atherosclerosis.
PMID:8645360 Yu PH, Zuo DM; Atherosclerosis 120 (1-2): 189-97 (1996)
/MILK/ ...The presence of volatile aliphatic amines ... in human breast milk and amniotic fluid /was measured/ to assess their role in neonatal hypergastrinemia. These volatile nitrogenous amino acid metabolites have been previously demonstrated to stimulate gastrin release in in vivo and in vitro laboratory preparations. ... The present study ... demonstrated that these gastrin-stimulatory volatile amines were present in significant concentrations in breast milk during the first several weeks after parturition and in amniotic fluid. The individual amines that were identified in both human milk and amniotic fluid samples were methylamine, dimethylamine, ethylamine, trimethylamine, propylamine, isobutylamine, and butylamine. This study provides indirect evidence to support the possibility that the hypergastrinemia measured in the fetus/neonate during the period immediately before and after birth may be attributable, in part, to the ingestion of fluid containing high concentrations of gastrin-stimulating amines.
PMID:1779307 Lichtenberger LM et al; J Pediatr Gastroenterol Nutr 13 (4): 342-6 (1991)
BACKGROUND: Dialysis adequacy is currently judged by measures of urea clearance. However, urea is relatively non-toxic and has properties distinct from large classes of other retained solutes. In particular, intracellularly sequestered solutes are likely to behave differently than urea. METHODS: We studied an example of this class, the aliphatic amine monomethylamine (MMA), in stable hemodialysis outpatients (n = 10) using an HPLC-based assay. RESULTS: Mean MMA levels pre-dialysis in end-stage renal disease subjects were 76 +/- 15 ug/L compared to 32 +/- 4 ug/L in normal subjects (n = 10) (P < 0.001). Mean urea reduction was 62% while the reduction ratio for MMA was 43% (P < 0.01). MMA levels rebounded in the 1 hour post-dialytic period to 85% of baseline, whereas urea levels rebounded only to 47% of baseline. MMA had a much larger calculated volume of distribution compared to urea, consistent with intracellular sequestration. Measures of intra-red blood cell (RBC) MMA concentrations confirmed greater levels in RBCs than in plasma with a ratio of 4.9:1. Because of the intracellular sequestration of MMA, we calculated its clearance using that amount removed from whole blood. Clearances for urea averaged 222 +/- 41 mL/min and for MMA 121 +/- 14 mL/min, while plasma clearance for creatinine was 162 +/- 20 mL/min (P < 0.01, for all differences). Using in vitro dialysis, in the absence of RBCs, solute clearance rates were similar: 333 +/- 6, 313 +/- 8 and 326 +/- 4 mL/min for urea, creatinine and MMA, respectively. These findings suggest that the lower MMA clearance relative to creatinine in vivo is a result of MMA movement into RBCs within the dialyzer blood path diminishing its removal by dialysis. CONCLUSION: In conclusion, we find that, in conventional hemodialysis, MMA is not cleared as efficiently as urea or creatinine and raise the possibility that RBCs may limit its dialysis not merely by failing to discharge it, but by further sequestering it as blood passes through the dialyzer.
PMID:20019016 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910329 Ponda MP et al; Nephrol Dial Transplant 25 (5): 1608-13 (2010)
In this study, we examined the effect of two creatine monohydrate supplementation regimes on 24-hr urinary creatine and methylamine excretion. Nine male participants completed two trials, separated by 6 weeks. Participants ingested 4 x 5 g x day(-1) creatine monohydrate for 5 days in one trial and 20 x 1 g x day(-1) for 5 days in the other. We collected 24-hr urine samples on 2 baseline days (days 1-2), during 5 days of supplementation (days 3-7), and for 2 days post-supplementation (days 8-9). Urine was assayed for creatine using high-performance liquid chromatography and methylamine using gas chromatography. Less creatine was excreted following the 20 x 1 g x day(-1) regime (49.25 +/- 10.53 g) than the 4 x 5 g x day(-1) regime (62.32 +/- 9.36 g) (mean +/- s; P < 0.05). Mean total excretion of methylamine (n = 6) over days 3-7 was 8.61 +/- 7.58 mg and 24.81 +/- 25.76 mg on the 20 x 1 g x day(-1) and 4 x 5 g x day(-1) regimes, respectively (P < 0.05). The lower excretion of creatine using 20 x 1 g x day(-1) doses suggests a greater retention in the body and most probably in the muscle. Lower and more frequent doses of creatine monohydrate appear to further attenuate formation of methylamine.
PMID:19437189 Sale C et al; J Sports Sci 27 (7): 759-66 (2009)
For more Absorption, Distribution and Excretion (Complete) data for Methylamine (8 total), please visit the HSDB record page.
PURPOSE: It has been claimed that oral creatine supplementation might have potential cytotoxic effects on healthy consumers by increasing the production of methylamine and formaldehyde. Despite this allegation, there has been no scientific evidence obtained in humans to sustain or disprove such a detrimental effect of this widely used ergogenic substance. METHODS: Twenty young healthy men ingested 21 g of creatine monohydrate daily for 14 consecutive days. Venous blood samples and 24-hr urine were collected before and after the 14th day of supplementation. Creatine and creatinine were analyzed in plasma and urine, and methylamine, formaldehyde, and formate were determined in 24-hr urine samples. RESULTS: Oral creatine supplementation increased plasma creatine content 7.2-fold (P < 0.001) and urine output 141-fold (P < 0.001) with no effect on creatinine levels. Twenty-four-hour urine excretion of methylamine and formaldehyde increased, respectively, 9.2-fold (P = 0.001) and 4.5-fold (P = 0.002) after creatine feeding, with no increase in urinary albumin output (9.78 +/- 1.93 mg/24 hr before, 6.97 +/- 1.15 mg/24 hr creatine feeding). CONCLUSION: This investigation shows that short-term, high-dose oral creatine supplementation enhances the excretion of potential cytotoxic compounds, but does not have any detrimental effects on kidney permeability. This provides indirect evidence of the absence of microangiopathy in renal glomeruli.
PMID:16260971 Poortmans JR et al; Med Sci Sports Exerc 37 (10): 1717-20 (2005)
Mono- and trimethylamines are converted to dimethylamine in the body.
Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. V4 708
The regulation of methylamine and formaldehyde metabolism in Arthobacter P1 was investigated in carbon-limited continuous cultures. Evidence was obtained that the synthesis of enzymes involved in the conversion of methylamine into formaldehyde and in formaldehyde fixation is induced sequentially in this organism.
Levering PR et al; Arch Microbiol 144 (3): 272-8 (1986)
The metabolism of methylamine has been investigated in the rat in order to elucidate the role of monoamine oxidase and intestinal bacteria in the metabolism of the compound. In a series of experiments in which short and long acting inhibitors of monoamine oxidase were administered either alone or in combination prior to methyl (14)C amine hydrochloride injection, the excretion of radioactivity in the expired air and the urine was examined to indirectly assess the role of monoamine oxidase in the metabolism of methylamine. The data ... provide indirect evidence to demonstrate that the effect of iproniazid, an inhibitor of methylamine oxidation, is mediated through enzyme systems separate from MAO systems which have been invoked as major contributors to metabolism of methylamine by other investigators. The bacterial oxidation of methylamine in the intestine plays a minor role in the overall metabolism of the compounds.
PMID:2867948 Dar MS et al; Gen Pharmacol 16 (6): 557-60 (1985)
For more Metabolism/Metabolites (Complete) data for Methylamine (7 total), please visit the HSDB record page.
Uremic toxins tend to accumulate in the blood either through dietary excess or through poor filtration by the kidneys. Most uremic toxins are metabolic waste products and are normally excreted in the urine or feces.
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