Dihydroxyacetone

90.08

90.08

202-494-5

O10DDW6JOO

24343

DTXSID0025072

Crystalline powder|Colorless, crystalline solid

2914400090

57.5

-1.4

Solid

1.3±0.1 g/cm3

90 °C

213.7°C at 760 mmHg

97.3±16.9 °C

1.455

>250 g/L (20 ºC)

Refrigerator (+4ºC)

4.35X10-5 mm Hg at 25 deg C

CHROMELIN ? DIHYDROXYACETONE ? 1,3DIHYDROXYACETONE ? 1,3-DIHYDROXYPROPANONE ? DIHYXAL ? NSC-24343 ? OTAN ? OXATONE ? SOLEAL ? 2PROPANONE, 1,3-DIHYDROXY- ? TRIULOSE ? VITICOLOR

Characteristic odor

Sweet, cooling taste

Henry's Law constant = 5.54X10-12 atm-cu m/mol at 25 °C (est)

Fairly hygroscopic ... the normal form is a dimer. When freshly prepared reverts rapidly to monomer in solution. The monomer is very soluble in water, alcohol, ether, acetone.|Hydroxyl radical reaction rate constant = 5.18X10-12 cu cm/molec-sec at 25 °C (est)

S24/25

Stable. Combustible. Hygroscopic.

P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, P501

H315

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Certification of this color additive when used as in drugs is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. Dihydroxyacetone may be safely used in amounts consistent with good manufacturing practice in externally applied drugs intended solely or in part to impart a color to the human body.|Certification of this color additive when used in cosmetics is not necessary for the protection of the public health, and therefore batches thereof are exempt from the certification pursuant to section 721(c) of the act. Dihydroxyacetone may be safely used in amounts consistent with good manufacturing practice in externally applied cosmetics intended solely or in part to impart a color to the human body.

|Warning|H315 (99.78%): Causes skin irritation [Warning Skin corrosion/irritation]|P261, P264, P271, P280, P302+P352, P304+P340, P305+P351+P338, P312, P321, P332+P313, P337+P313, P362, P403+P233, P405, and P501|Aggregated GHS information provided by 1450 companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

... 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< 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< 0.05). Fasting and postoral glucose, plasma insulin, glucagon, and C peptide levels were unaffected by DHP. /Mixture of dihydroxyacetone and pyruvate/.|Dihydroxyacetone (DHA) effectively antagonized the lethal effect of cyanide in mice and rabbits, particularly if administered in combination with thiosulfate. Oral DHA (2 and 4 g/kg) given to mice 10 min before injection (ip) of cyanide increased the LD50 values of cyanide from 5.7 mg/kg to 12 and 17.6 mg/kg, respectively. DHA prevented cyanide-induced lethality most effectively, if given orally 10-15 min before injection of cyanide. A combination of pretreatment with oral DHA (4 g/kg) and post-treatment with sodium thiosulfate (1 g/kg) increased the LD50 of cyanide by a factor of 9.9. Furthermore, DHA given intravenously to rabbits 5 min after subcutaneous injection of cyanide increased the LD50 of cyanide from 6 mg/kg to more than 11 mg/kg, while thiosulfate (1 g/kg) given intravenously 5 min after cyanide injection increased the LD50 of cyanide only to 8.5 mg/kg. DHA also prevented the convulsions that occurred after cyanide intoxication.|Potassium cyanide (CN) intoxication in mice was found to be effectively antagonized by dihydroxyacetone (DHA), particularly if administered in combination with another CN antidote, sodium thiosulfate. Cyanide-induced convulsions were also prevented by DHA treatment, either alone or in combination with thiosulfate. Injection (ip) of DHA (2 g/kg) 2 min after or 10 min before CN (sc) increased LD50 values of CN (8.7 mg/kg) by factors of 2.1 and 3.0, respectively. Treatment with a combination of DHA and thiosulfate after CN increased the LD50 by a factor of 2.4. Pretreatment with a combination of DHA and thiosulfate (1 g/kg) increased the LD50 of CN to 83 mg/kg. Administration of alpha-ketoglutarate (2.0 g/kg), but not pyruvate, 2 min after CN increased the LD50 of CN by a factor of 1.6. Brain, heart and liver cytochrome oxidase activities were also measured following in vivo CN treatment with and without DHA. Pretreatment with DHA prevented the inhibition of cytochrome oxidase activity by CN and treatment with DHA after CN accelerated the recovery of cytochrome oxidase activity, especially in brain and heart homogenates ...

Dihydroxyacetone's production and use as a chemical intermediate(1) and as an artificial tanning agent(2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 23(SRC), determined from a log Kow of -1.95(2), and a regression-derived equation(3) indicates that dihydroxyacetone is expected to have very high mobility in soil(SRC). Volatilization of dihydroxyacetone from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.5X10-12 atm-cu m/mole(SRC), derived from its vapor pressure, 4.35X10-5 mm Hg(2), and water solubility, 9.3X10+5 mg/L(2). Dihydroxyacetone is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(2). Biodegradation data in soil were not available(SRC, 2012).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 23(SRC), determined from a log Kow of -1.95(2) and a regression derived equation(3), indicates that dihydroxyacetone is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 5.5X10-12 atm-cu m/mole(SRC), derived from its vapor pressure, 4.35X10-5 mm Hg(2), and water solubility, 9.3X10+5 mg/L(2). According to a classification scheme(5), an estimated BCF of 9(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data in water were not available(SRC, 2012).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dihydroxyacetone, which has a vapor pressure of 4.35X10-5 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase dihydroxyacetone is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2 days(SRC), calculated from its rate constant of 5.2X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Dihydroxyacetone does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of dihydroxyacetone with photochemically-produced hydroxyl radicals has been estimated as 5.2X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Dihydroxyacetone is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Dihydroxyacetone contains does not contain chromophores that absorb at wavelengths >290 nm(2) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 9 was calculated in fish for dihydroxyacetone(SRC), using a log Kow of -1.95(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Koc of dihydroxyacetone is estimated as 9(SRC), using a log Kow of -1.95(1) and a regression-derived equation(2). According to a classification scheme(2), this estimated Koc value suggests that dihydroxyacetone is expected to have very high mobility in soil. [

The Henry's Law constant for dihydrocyacetone is estimated as 5.5X10-12 atm-cu m/mole(SRC) derived from its vapor pressure, 4.35X10-5 mm Hg(1), and water solubility, 9.3X10+5 mg/L(1). This Henry's Law constant indicates that dihydrocyacetone is expected to be essentially nonvolatile from water surfaces(2). Dihydroxyacetone's Henry's Law constant indicates that volatilization from moist soil surfaces not may occur(SRC). Dihydroxyacetone is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

Occupational exposure to dihydroxyacetone may occur through inhalation and dermal contact with this compound at workplaces where dihydroxyacetone is produced or used. Use data indicate that the general population may be exposed to dihydroxyacetone via dermal contact with consumer products containing dihydroxyacetone. (SRC)

/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.|/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.|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 ...|/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.|/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/.

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.

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.

...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.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Ketones and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . For contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Ketones and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Ketones and related compounds/

/HUMAN EXPOSURE STUDIES/ ... 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< 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< 0.05). Fasting and postoral glucose, plasma insulin, glucagon, and C peptide levels were unaffected by DHP. /Mixture of dihydroxyacetone and pyruvate/.|/ALTERNATIVE and IN VITRO TESTS/ ... The effects of dihydroxyacetone (DHA) on cell survival and proliferation of a human keratinocyte cell line, HaCaT /were investigated/. Dose- and time-dependent morphological changes, chromatin condensation, cytoplasmic budding and cell detachment were seen in cells treated with DHA. Several dead cells were observed after long-time (24 hr) incubation with 25 mM DHA or more. Furthermore, an extensive decline in proliferation was observed 1 day after DHA exposure for 24 hr. When applied in different concentrations (5-50 mM) and for different time periods (1, 3 or 24 hr) DHA caused a G(2)/M block after the cyclin B(1) restriction point. Exit from this cell-cycle block was associated with massive apoptosis, as revealed by a clonogenic assay, TUNEL staining and electron microscopy. Furthermore, DHA caused DNA damage as revealed by the alkaline comet assay.

1,3 Dihydroxy 2 Propanone

Man-Tan, Oxatone, Tanorama, Q.T (Quick Tan); Tan Tone; Magic Tan|Otan, Soleal

2-Propanone, 1,3-dihydroxy-: ACTIVE

Analyte: dihydroxyacetone; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards|Analyte: dihydroxyacetone; matrix: chemical identification; procedure: liquid chromatography retention factor value with comparison to standards|Analyte: dihydroxyacetone; matrix: chemical purity; procedure: dissolution in water; addition of periodic acid; addition of sodium bicarbonate, potassium iodide, and starch; titration with sodium arsenite with comparison to standards

Cosmetics -> Reducing; Tanning