X
1. 1,3 Dihydroxy 2 Propanone
2. 1,3-dihydroxy-2-propanone
3. Chromelin
4. Vitadye
1. 1,3-dihydroxyacetone
2. 96-26-4
3. 1,3-dihydroxypropan-2-one
4. 1,3-dihydroxy-2-propanone
5. Glycerone
6. Chromelin
7. Viticolor
8. Dihyxal
9. Oxantin
10. Oxatone
11. Triulose
12. Soleal
13. Otan
14. 2-propanone, 1,3-dihydroxy-
15. 1,3-dihydroxypropanone
16. 1,3-dihydroxydimethyl Ketone
17. Vitadye
18. Nsc-24343
19. Dihydroxy-acetone
20. Bis(hydroxymethyl) Ketone
21. 2-propanone, 1,3-dihydroxy
22. Ketochromin
23. Ccris 4899
24. Brn 1740268
25. Unii-o10ddw6joo
26. O10ddw6joo
27. Ai3-24477
28. Einecs 202-494-5
29. Fema No. 4033
30. Chebi:16016
31. Hsdb 7513
32. Dihydroxyacetone [usp]
33. 1,3-propanediol-2-one
34. Mfcd00004670
35. Alpha,alpha'-dihydroxyacetone
36. Dtxsid0025072
37. Ec 202-494-5
38. 4-01-00-04119 (beilstein Handbook Reference)
39. Dihydroxyacetone (usp)
40. Dihydroxyacetone (mart.)
41. Dihydroxyacetone [mart.]
42. Dihydroxyacetone (usp-rs)
43. Dihydroxyacetone [usp-rs]
44. Dihydroxyacetone (usp Monograph)
45. Dihydroxyacetone [usp Monograph]
46. 1,3 Dihydroxy 2 Propanone
47. Protosol
48. Aliphatic Ketone
49. Dihydroxypropanone
50. Chromelin (tn)
51. 1,3-dihydroxyaceton
52. 1.3-dihydroxyacetone
53. A,a'-dihydroxyacetone
54. 1,3-dihyroxy-acetone
55. 1,3-dihydroxy-acetone
56. Dihydroxy Acetone
57. 2-propanone,3-dihydroxy-
58. Bmse000144
59. Dihydroxyacetone [mi]
60. 1, 3-dihydroxypropan-2-one
61. 1,3-dihydroxyacetone (dha)
62. Dihydroxyacetone [fhfi]
63. Dihydroxyacetone [hsdb]
64. Dtxcid405072
65. Dihydroxyacetone [vandf]
66. Chembl1229937
67. Dihydroxyacetone [who-dd]
68. Hy-y0335
69. Nsc24343
70. Akos005259385
71. Cs-w019614
72. Db01775
73. Gs-3764
74. Sb83769
75. Sy038299
76. D5818
77. Ft-0649652
78. Ns00004299
79. C00184
80. D07841
81. En300-121747
82. S12381
83. A845572
84. Q409618
85. J-503909
86. Q-101302
87. F0001-2767
88. Z1255442144
89. 08cb5e10-c843-45ee-8556-4313c8e0bea2
90. Inchi=1/c3h6o3/c4-1-3(6)2-5/h4-5h,1-2h
| Molecular Weight | 90.08 g/mol |
|---|---|
| Molecular Formula | C3H6O3 |
| XLogP3 | -1.4 |
| Hydrogen Bond Donor Count | 2 |
| Hydrogen Bond Acceptor Count | 3 |
| Rotatable Bond Count | 2 |
| Exact Mass | g/mol |
| Monoisotopic Mass | g/mol |
| Topological Polar Surface Area | 57.5 |
| Heavy Atom Count | 6 |
| Formal Charge | 0 |
| Complexity | 44 |
| 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 objective of this study was/ to evaluate the properties of dihydroxyacetone (DHA) in a new formulation for the treatment of vitiligo on exposed areas. ... Ten patients suffering from vitiligo affecting the face and/or hands /were treated/ with a newly introduced, commercially available self-bronzing cream containing DHA 5%. DHA was applied every second day. The characteristic pigmentation showed very satisfactory cosmetic results in 8 out of 10 patients after 2 weeks of treatment. The new DHA formulation is a practical and well-accepted treatment modality.
PMID:11701979 Fesq H et al; Dermatology 203 (3): 241-3 (2001)
/EXPL THER/ Dihydroxyacetone (DHA), a three-carbon sugar, is the browning ingredient in commercial sunless tanning formulations. ... In this work, the in vitro antifungal activity of dihydroxyacetone was tested against causative agents of dermatomycosis, more specifically against dermatophytes and Candida spp. The antifungal activity was determined by the broth microdilution method according to the Clinical and Laboratory Standards Institute guidelines for yeasts and filamentous fungi. The data obtained show that the fungicidal activity varied from 1.6 to 50 mg/mL. DHA seems to be a promising substance for the treatment of dermatomycosis because it has antifungal properties at the same concentration used in artificial suntan lotions. Therefore, it is a potential low-toxicity antifungal agent that may be used topically because of its penetration into the corneal layers of the skin.
PMID:20936361 Stopiglia CD et al; Mycopathologia 171 (4): 267-71 (2011)
During seven months of a clinical trial in spring, summer, and fall, 30 UVA/B/Soret band-photosensitive patients used sequential topical applications of dihydroxyacetone (DHA) followed by naphthoquinone only at bedtime and received excellent photoprotection without a single therapeutic failure or loss of any patient to follow-up. Eighteen of the 30 patients extended the limits of their photoprotection repeatedly over a seven-month period to tolerate without sunburns six to eight hrs of midday sunlight under all kinds of occupational and recreational environmental conditions ...
PMID:16037237 Fusaro RM and Rice EG; Ann N Y Acad Sci 1043:174-83 (2005)
/EXPTL THER/ ... the protection with topical application of dihydroxyacetone (DHA) against solar UV-induced skin carcinogenesis in lightly pigmented hairless hr/hr C3H/Tif mice /was investigated/. ... Three groups of mice were UV-exposed four times a wk to a dose-equivalent of four times the standard erythema dose (SED), without or with application of 5 or 20% DHA only twice a week. Similarly, three groups of mice were treated with DHA and irradiated with a high UV dose (8 standard erythema dose), simulating a skin burn. Two groups (controls) were not irradiated, but either left untreated or treated with 20% DHA alone. The UV-induced skin pigmentation by melanogenesis could easily be distinguished from DHA-induced browning and was measured by a non-invasive, semi-quantitative method. Application of 20% DHA reduced by 63% the pigmentation produced by 4 standard erythema dose, however, only by 28% the pigmentation produced by 8 standard erythema dose. Furthermore, topical application of 20% DHA significantly delayed the time to appearance of the first tumor >or=1mm (P=0.0012) and the time to appearance of the third tumor (P=2 x 10(-6)) in mice irradiated with 4 standard erythema dose. However, 20% DHA did not delay tumor development in mice irradiated with 8 standard erythema dose. Application of 5% DHA did not influence pigmentation or photocarcinogenesis.
PMID:14644361 Petersen AB et al; Mutat Res 542 (1-2): 129-38 (2003)
/EXPTL THER/ ... Consumption of dihydroxyacetone and pyruvate (DHP) increases muscle extraction of glucose in normal men. To test the hypothesis that these three-carbon compounds would improve glycemic control in diabetes the effect of DHP on plasma glucose concentration, turnover, recycling, and tolerance in 7 women with noninsulin-dependent diabetes /was evaluated/. The subjects consumed a 1,500-calorie diet (55% carbohydrate, 30% fat, 15% protein), randomly containing 13% of the calories as DHP (1/1) or Polycose (placebo; PL), as a drink three times daily for 7 days. On the 8th day, primed continuous infusions of [6-(3)H]-glucose and [U-(14)C]-glucose were begun at 05.00 hr, and at 09.00 hr a 3-hr glucose tolerance test (75 g glucola) was performed. Two weeks later the subjects repeated the study with the other diet. The fasting plasma glucose level decreased by 14% with DHP (DHP = 8.0 + or - 0.9 mmol/L; PL = 9.3 + or - 1.0 mmol/L, p less than 0.05) which accounted for lower postoral glucose glycemia (DHP = 13.1 + or - 0.8 mmol/L, PL = 14.7 + or - 0.8 mmol/L, p less than 0.05). [6-(3)H]-glucose turnover (DHP = 1.50 + or - 0.19 mg/kg-L/min, PL = 1.77 + or - 0.21 mmg/kg-L/min, p less than 0.05) and glucose recycling, the difference in [6-(3)H]-glucose and [U-(14)C]-glucose turnover rates, decreased with DHP (DHP = 0.25 + or - 0.07 mg/kg-L/min, PL = 0.54 + or - 0.10 mg/kg-L/min, p less than 0.05). Fasting and postoral glucose, plasma insulin, glucagon, and C peptide levels were unaffected by DHP. /Mixture of dihydroxyacetone and pyruvate/.
PMID:2132162 Stanko RT et al; Clin Physiol Biochem 8 (6): 283-8 (1990)
The present study investigated the fate of dihydroxyacetone (DHA) in an in vitro absorption study. In these studies, human ... skin penetration and absorption were determined over 24 or 72 hr in flow-through diffusion cells. ... For DHA, penetration studies found approximately 22% of the applied dose remaining in the skin (in both the stratum corneum and viable tissue) as a reservoir after 24 hr. Little of the DHA that penetrates into skin is actually available to become systemically absorbed.
PMID:15020193 Yourick JJ et al; Toxicol Appl Pharmacol 195 (3): 309-20 (2004)
Several bacteria use glycerol dehydrogenase to transform glycerol into dihydroxyacetone (DHA). DHA is subsequently converted into DHA phosphate (DHA-P) by an ATP- or phosphoenolpyruvate (PEP)-dependent DHA kinase. Listeria innocua possesses two potential PEP-dependent Dha kinases. One is encoded by 3 of the 11 genes forming the glycerol (gol) operon. This operon also contains golD (lin0362), which codes for a new type of DHA-forming NAD(+)-dependent glycerol dehydrogenase. The subsequent metabolism of DHA requires its phosphorylation via the PEP:sugar phosphotransferase system components enzyme I, HPr, and EIIA(DHA)-2 (Lin0369). P-EIIA(DHA)-2 transfers its phosphoryl group to DhaL-2, which phosphorylates DHA bound to DhaK-2. The resulting Dha-P is probably metabolized mainly via the pentose phosphate pathway, because two genes of the gol operon encode proteins resembling transketolases and transaldolases. In addition, purified Lin0363 and Lin0364 exhibit ribose-5-P isomerase (RipB) and triosephosphate isomerase activities, respectively. The latter enzyme converts part of the DHA-P into glyceraldehyde-3-P, which, together with DHA-P, is metabolized via gluconeogenesis to form fructose-6-P. Together with another glyceraldehyde-3-P molecule, the transketolase transforms fructose-6-P into intermediates of the pentose phosphate pathway. The gol operon is preceded by golR, transcribed in the opposite orientation and encoding a DeoR-type repressor. Its inactivation causes the constitutive but glucose-repressible expression of the entire gol operon, including the last gene, encoding a pediocin immunity-like (PedB-like) protein. Its elevated level of synthesis in the golR mutant causes slightly increased immunity against pediocin PA-1 compared to the wild-type strain or a pedB-like deletion mutant.
PMID:22773791 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3430356 Monniot C et al; J Bacteriol 194 (18): 4972-82 (2012)
...The toxicity of dihydroxyacetone appears to be due to its intracellular conversion to an aldehyde compound, presumably methylglyoxal, since the glyoxalase mutant becomes sensitive to dihydroxyacetone. Based on information that gldA is preceded in an operon by the ptsA homolog and talC gene encoding fructose 6-phosphate aldolase, this study proposes that the primary role of gldA is to remove toxic dihydroxyacetone by converting it into glycerol.
PMID:18179582 Subedi KP et al; FEMS Microbiol Lett 279 (2): 180-7 (2008)
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