Xylitol

152.15

152.15

1720523

201-788-0

VCQ006KQ1E|353ZQ9TVDA

DTXSID7042514

Monoclinic crystals from alcohol

2905491000

101

-2.5

White Crystalline Powder

1.5±0.1 g/cm3

93.5 °C

216 °C

261.9±21.9 °C

1.571

H2O: soluble

2-8°C

2.47X10-3 mm Hg at 25 deg C (est)

LD50 orally in mice: approx 22 g/kg (Salminen)

Relative sweetness equal to sucrose

5 to 7 (10 % w/v aqueous solution)

Henry's Law constant = 1.5X10-11 atm-cu m/mole at 25 °C (est)

136.3 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|135.3 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|122.4 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]|140.79 Ų [M+Na]+ [CCS Type: DT, Method: stepped-field]|127.92 Ų [M-H]- [CCS Type: DT, Method: stepped-field]|136.2 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|135.4 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|125.8 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|124.8 Ų [M-H]- [CCS Type: DT, Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]|126.2 Ų [M-H]-

Orthrhombic needles from tetrahydrofuran, prisms from ethanol; mp: 93-94.5 °C; density: 1.52. Solubility (g/100 g solution): absolute methanol 6.0; absolute ethanol 1.2; water 64.2 /Stable form/|Hydroxyl radical reaction rate constant = 3.96X10-11 cu cm/molec-sec at 25 °C (est)

NONH for all modes of transport

2

36/37/38

24/25-36-26

ZF0800000

Xi

Xylitol is stable to heat but is marginally hygroscopic. Caramelization can occur only if it is heated for several minutes near ist boiling point. Milled and specialized granulated grades of xylitol have a tendency to cake and should therefore be used within 9 to 12 months. Aqueous xylitol solutions have been reported to be stable, even on prolonged heating and storage.

SRP: Criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Xylitol is a food additive permitted for direct addition to food for human consumption, as long as 1) the quantity of the substance added to food does not exceed the amount reasonably required to accomplish its intended physical, nutritive, or other technical effect in food, and 2) any substance intended for use in or on food is of appropriate food grade and is prepared and handled as a food ingredient.|Food labeling. Health claims: dietary noncariogenic carbohydrate sweeteners and dental caries. ... Eligible noncariogenic carbohydrate sweeteners are the sugar alcohols xylitol, sorbitol, mannitol, maltitol, isomalt, lactitol, hydrogenated starch hydrolysates, hydrogenated glucose syrups, and erythritol, or a combination of these.

Airborne exposure should be controlled primarily by engineering controls such as general dilution ventilation, local exhaust ventilation, or process enclosure. Local exhaust ventilation is generally preferred to general exhaust because it can control the contaminant at its source, preventing dispersion into the work area. An industrial hygiene survey involving air monitoring may be used to determine the effectiveness of engineering controls. Effectiveness of engineering controls intended for use with highly potent materials should be assessed by use of nontoxic surrogate materials.|Where respirators are deemed necessary to reduce or control occupational exposures, use NIOSH-approved respiratory protection and have an effective respirator program in place (applicable U.S. regulation OSHA 29 CFR 1910.134).

Water spray, dry chemical, carbon dioxide, or foam as appropriate for surrounding fire and materials.|As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing.

Wear approved respiratory protection, chemically compatible gloves, and protective clothing. Wipe up spillage or collect spillage using a high-efficiency vacuum cleaner. Avoid breathing dust. Place spillage in appropriately labeled container for disposal. Wash spill site.

SRP: The scientific literature for the use of contact lenses by industrial workers is inconsistent. The benefits or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|This material is assumed to be combustible. As with all dry powders, it is advisable to ground mechanical equipment in contact with dry material to dissipate the potential buildup of static electricity.|As a general rule, when handling USP Reference Standards, avoid all contact and inhalation of dust, mists, and/or vapors associated with this material. Clean equipment and work surfaces with suitable detergent or solvent after use. After removing gloves, wash hands and other exposed skin thoroughly.|Chemically compatible. For handling solutions, ensure that the glove material is protective against the solvent being used. Use handling practices that minimize direct hand contact. Employees who are sensitive to natural rubber (latex) should use nitrile or other synthetic nonlatex gloves. Use of powdered latex gloves should be avoided due to the risk of latex allergy.|For more Preventive Measures (Complete) data for Xylitol (6 total), please visit the HSDB record page.

Xylitol may... also be an irritant to the eyes. Eye protection and gloves are recommended. Conventional dust-control practices should be employed.

Oral LD50 is 16500 mg/kg in rat [MSDS]. At high dosages, xylitol can cause diarrhea in children at 45 g/d and 100 g/d in adults.

Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF-alpha and IL-1beta expression. The kinetics of TNF-alpha and IL-1beta levels in culture supernatant after LPS treatment showed peak values at 1 hr (TNF-alpha) and 2 to 4 hr (IL-1beta), respectively. NF-kappaB, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF-kappaB activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF-kappaB). Pretreatment with xylitol inhibited LPS-induced TNF-alpha and IL-1beta gene expression and protein synthesis. LPS-induced mobilization of NF-kappaB was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.|Oxalate levels in the plasma and urine fractions of fasted normal, oxythiamin treated (20 mg/kg) and 4-deoxypyridoxine treated (300 mg/kg) rabbits were determined following infusion with either xylitol or glucose at a dose of 2 g/kg body weight. Biochemical determinations showed that transient thiamin or pyridoxine deficient states had been induced in the antivitamin treated rabbits. In the first 24 hour following infusion with either carbohydrate, urinary oxalate levels remained within the normal range for all groups. Oxythiamin hastened the appearance of the transient, elevation in plasma oxalate concentrations seen in rabbits after infusion with glucose. After xylitol infusion, the elevation of plasma oxalate was not significantly above normal. 4-Deoxypyridoxine enhanced peak plasma oxalate levels above those of controls for both sugars. Glucose, at an equivalent dose to xylitol, resulted in higher plasma oxalate levels than xylitol for all groups. Infusions of [U-(14)C]xylitol and [U-(14)C]glucose solutions into 4-deoxypyridoxine treated rabbits demonstrated a conversion of the administered radioactive carbon into (14)C oxalate of 0.01% with a high dilution of the specific activity. The results suggest that oxalate production from xylitol is negligible; any toxicity related to xylitol administration is not a consequence of oxalate production.|The absorption of (14)C -labelled oxalic acid was studied in Wistar rats, CD-1 mice and NMRI mice. Oxalic acid in solution was given to the animals by gavage either with water alone or with 0.625 g/kg b.w. of xylitol. Both xylitol-adapted animals and animals not previously exposed to xylitol were used. Adaption to xylitol diets enhanced the absorption and urinary excretion of the label (oxalic acid) in both strains of mice but not in rats. Earlier studies have indicated a high incidence of bladder calculi in mice but not in rats fed high amounts of xylitol. The results of the present study offer one likely explanation for the increased formation of bladder calculi as a result of oversaturation of urine with oxalate.|Xylitol was investigated for its ability to ameliorate hemolytic anemia induced by acetylphenylhydrazine in rabbits. Animal experiments were performed using two different concentrations of xylitol, a 5% and a 10% solution with a total dose of 2 g/kg body weight and infusion rates of 10 mg and 20 mg xylitol per kg body weight per minute respectively. Two doses of acetylphenylhydrazine (APH), 5 and 10 mg per kg, were injected intraperitoneally as hemolytic inducers in different groups of rabbits. All the rabbits infused with xylitol showed significantly less acute APH-induced hemolysis. The isotonic 5% xylitol solution was found to maintain and restore the hematological parameters (packed cell volume, hemoglobin concentration, reduced glutathione (GSH) content, and reticulocyte counts) better than the 10% xylitol solution. Increased (51)Cr-red cell survival confirmed the beneficial effect of xylitol. The survival of erythrocytes as represented by chromium-labeling in rabbits infused with 5% xylitol after treatment with 10 mg/kg APH increased from about 33% (the survival of red cells in rabbits injected with APH alone) to 67% of normal rabbits' red cell survival. Erythrocytes in APH-treated animals took up xylitol more readily than erythrocytes from control animals. Our results in rabbits suggest that (1) non-toxic dosage of xylitol is effective in ameliorating the hemolytic episode induced by APH, (2) there is a dose relationship between the hemolytic effect induced by APH and the preventive effect offered by xylitol, (3) drug-challenged cells effectively acquired two to three fold more xylitol to compensate for the cellular needs than that of the normal cells, and (4) sufficient xylitol (55 mg/dL) to act as substrate for xylitol dehydrogenase was recovered intracellularly in drug-challenged rabbit erythrocyte in vivo, in spite of a low plasma (<30 mg/dL) concentration of the substrate. This antihemolytic affect of xylitol is likely accomplished through NADPH generation, which maintains the level of GSH and protects the hemoglobin and other structural and functional proteins against peroxidative damage.|The effects of oral administration of xylitol on the rate of ethanol elimination and on the ethanol-induced changes in blood concentrations of lactate and pyruvate were studied in seven healthy male subjects. Xylitol (1.0 g/kg body weight) was administered orally and ethanol (0.8 g/kg body weight) intravenously. In the control experiments glucose was given instead of xylitol. Xylitol had no significant effect on the rate of ethanol elimination or on the ethanol-induced increase in the blood lactate concentration. The ethanol-induced changes in the lactate/pyruvate ratio were not affected by xylitol. It is suggested that the ineffectiveness of xylitol is due to its low concentration in the liver after oral administration. Ethanol induced a 5-10-fold increase in the blood concentration of xylitol. This is most probably due to inhibition of xylitol oxidation in the liver by the ethanol-induced reduction in the hepatic redox state. The clinical significance of this finding is unknown.

LD50 Rabbit iv 4 g/kg|LD50 Rabbit oral 16.5 g/kg|LD50 Rat iv 10.8 g/kg|LD50 Rat oral 17.3 g/kg|For more Non-Human Toxicity Values (Complete) data for Xylitol (21 total), please visit the HSDB record page.

No pharmacokinetic data available.

Xylitol's production and use as a bulk sweetener, in dietetic foods, pharmaceutical preparations, and solutions for parenteral nutrition(1) 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 10(SRC), determined from a structure estimation method(2), indicates that xylitol is expected to have very high mobility in soil(SRC). Volatilization of xylitol from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.5X10-11 atm-cu m/mole(SRC), using a fragment constant estimation method(3). Xylitol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.5X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(4). An 82% of theoretical BOD in 2 weeks using an activated sludge inoculum in the Japanese MITI test(5) suggests that biodegradation may be an important environmental fate process in soil(SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that xylitol is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 1.5X10-11 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of -2.56(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). An 82% of theoretical BOD in 2 weeks using an activated sludge inoculum in the Japanese MITI test(8) suggests that biodegradation may be an important environmental fate process in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), xylitol, which has an estimated vapor pressure of 2.5X10-3 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase xylitol 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 3 hours(SRC), calculated from its rate constant of 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Xylitol 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 xylitol with photochemically-produced hydroxyl radicals has been estimated as 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 3 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Xylitol is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Xylitol 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 3 was calculated in fish for xylitol(SRC), using an estimated log Kow of -2.56(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).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of xylitol can be estimated to be 10(SRC). According to a classification scheme(2), this estimated Koc value suggests that xylitol is expected to have very high mobility in soil.

The Henry's Law constant for xylitol is estimated as 1.5X10-11 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that xylitol is expected to be essentially nonvolatile from water and moist soil surfaces(2). Xylitol is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 2.5X10-3 mm Hg(SRC), determined from a fragment constant method(3).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 984 workers (796 of these were female) were potentially exposed to xylitol in the US(1). Occupational exposure to xylitol may occur through inhalation and dermal contact with this compound at workplaces where xylitol is produced or used. Use data indicate that the general population may be exposed to xylitol via ingestion of and dermal contact with consumer products containing xylitol(SRC).

Indicated for use as a sugar substitute, and oral hygiene active ingredient.|Cardioplegia

Sweetening Agents

There has been evidence of xylitol in dental hygiene in reducing dental caries disease and also reversing the process of early caries. Xylitol increases salivary flow and pH, reduces the levels of _Streptococcus mutans_ in plaque and saliva and reduces the adhesion on the microorganism to the teeth surface. _Streptococcus mutans_ is the main target plaque microorganism, but xylitol may potentially have inhibitory actions against several other bacterial species. It prevents a shift of the bacterial community towards a more cariogenic microflora in oral environment. Oral ingestion of xylitol causes a smaller rise in plasma glucose and insulin concentrations than does the ingestion of glucose in healthy men and diabetics.

Substances that sweeten food, beverages, medications, etc., such as sugar, saccharine or other low-calorie synthetic products. (From Random House Unabridged Dictionary, 2d ed) (See all compounds classified as Sweetening Agents.)

Xylitol is absorbed in the small intestine via passive diffusion with a slow absorption rate.|No pharmacokinetic data available.|Five healthy human volunteers (two males and three females) received an orange flavored drink containing 30 g xylitol with breakfast. Before dosing, urine was collected for 24 hr and collections were continued 24 hr after the dose of xylitol. During the collection period no foods rich in oxalate were permitted. No significant changes in urinary oxalate excretion could be detected.|Diets containing 20% of xylitol or one of the following carbohydrates: glucose, fructose, sucrose, xylose, sorbitol or mannitol were fed to groups of five Wistar rats for seven days. The rats were fasted for 12 hr and given a 5 uCi dose of U(14)C-oxalic acid mixed with 0.625 g/kg of xylitol or respective carbohydrate. Urine and feces were collected for 72 hr and counted for recovery of activity. Ten rats were gradually adapted to 20% xylitol diets. After a 12-hr fast these rats and 20 controls received 5 uCi of U(14)C-oxalic acid mixed with water only or together with 0.625 g/kg xylitol/body weight. Urine and feces were collected from five rats/group; tail vein blood from the other rats at intervals up to 24 hours. Urinary excretion of the label was virtually identical in all groups. The mean excretion of label in feces of control rats receiving oxalic acid was significantly lower (P <0.001) than in control rats receiving oxalate alone, or xylitol adapted rats receiving oxalate with xylitol (fecal recoveries were 77.8 and 83% respectively). The urinary excretion of label was also significantly higher among control rats receiving oxalate with xylitol when compared to control rats receiving oxalate alone. However, xylitol adapted rats excreted a significantly smaller proportion of oxalate in urine compared to controls receiving oxalate alone. The mean plasma levels of radioactivity in control rats receiving oxalic acid with xylitol were significantly higher (P <0.05) immediately after the start of the study when compared to controls receiving oxalic acid with water only or xylitol adapted rats. When samples of plasma, urine and feces were analyzed by use of thin layer chromatography, the major part of the radioactivity was recovered as oxalic acid.|Male (30) and female (20) CD-1 mice were either gradually adapted to 20% xylitol diets or fed a control diet. After a 12-hour fast the mice received a single oral dose of 2 uCi of U(14)C-oxalic acid in water or in an xylitol solution (a total dose of 0.625 g/kg bw). For five xylitol adapted male mice the oxalic acid dose was given with sorbitol (0.625 g/kg bw) and for another group of five with mannitol (0.625 g/kg bw). Urine and feces were collected at intervals for 72 hours to monitor the excretion of the label. ... Adaptation of male mice to 20% dietary xylitol increased the urinary excretion of the label fourfold (4.5 versus 20%). No major changes were seen in fecal excretion. Both sorbitol and mannitol increased the urinary excretion of the label while only sorbitol also affected fecal excretion of the label. Urinary excretion of oxalic acid was significantly higher in xylitol adapted mice when compared to controls receiving oxalic acid only. Even greater urinary recovery of label was observed in control mice receiving oxalic acid with xylitol. In female mice xylitol appeared to induce an even more pronounced increase in oxalic acid excretion.|Six groups of three Sprague-Dawley male weanling rats received semi-synthetic diets for 28 days; four of the groups were pyridoxine deficient. Diets contained either 50% glucose by weight or 30% glucose and 20% fructose. On day 28 the rats were injected three times at spaced intervals with either 15% glucose; 10% xylitol + 5% glucose; 15% fructose; or 10% xylitol + 5% fructose. Urine was collected on days 28 and 29 and rats were sacrificed and livers collected 30 minutes after a final injection on day 30. The final body weights for the rats show that the group with the best growth received fructose + xylitol injections and was pyridoxine adequate (mean weight 216.6 g) versus the group receiving fructose + fructose injection (15%) and were pyridoxine deficient (119.7 g). The poorest growing groups received glucose diets only and either xylitol or glucose and glucose injections, and were pyridoxine deficient (107.1 g, 103.1 g). The rats on the pyridoxine deficient diets tended to excrete more oxalate and have higher liver oxalate levels. Within the pyridoxine deficient group only, rats injected with xylitol tended to excrete more oxalate and have higher liver oxalate levels, but these differences were not significant. Fructose had no effect on oxalate excretion or liver oxalate levels in the rats injected with xylitol.|For more Absorption, Distribution and Excretion (Complete) data for Xylitol (10 total), please visit the HSDB record page.

In mammals, xylitol is mainly metabolized in the liver where it is oxidized to D-xylulose by xylitol dehydrogenase and cofactor NAD. D-xyluose is further phosphorylated and metabolized by xylulose kinase to xylulose 5-phosphate (Xu5P), an intermediate of the nonoxidative branch of the pentose phosphate pathway. Xu5P is reported to activate nuclear transport and the DNA-binding activities of carbohydrate response element binding protein (ChREBP) via activation of activation of protein phosphatase 2A (PP2A) _in vitro_. Activation of ChREBP thereby upregulates the gene transcription of lipogenic enzymes in vitro, which may stimulate lipogenesis in the liver.|The biochemical pathways for formation of oxalate after intravenous injection of xylitol in humans were studied using enzymes derived from human liver. It was concluded that metabolic pathways based on a combination of the transketolase, fructokinase, and aldolase reactions can account for the production of glucose, lactate, tertronates (D-threonic and D-erythronic acids) and oxalate (precursors) during the metabolism of xylitol administered parenterally.|After xylitol ingestion increase of serum lactate concentration and lactate-pyruvate ratio was observed, but to a degree less than after glucose. /Investigators/ also found a marked increase of alpha-dihydroxybutyrate. Complete metabolism of xylitol produces 35 equivalents of ATP compared to 32 from glucose.|/In humans/ exogenous xylitol enters the pathway by conversion to D-xylulose by a nonspecific cytoplasmic polyol dehydrogenase. Phosphorylation then yields D-xylulose phosphate, the link between the glucuronic acid and the pentose phosphate pathways; the latter leads to the formation of glyceraldehyde-3-phosphate and fructose-6-phosphate, intermediate metabolites of the Embden-Meyerhof (glycolytic) pathway. Thus xylitol can be metabolized via glucose-6-phosphate to glycogen and pyruvate or lactate via the citric acid cycle to CO2. Xylitol is mainly metabolized in the liver (80% to glucose only 20%) but a small amount also in kidney, myocardium, erythrocytes, adrenal, brain, lungs and adipose tissue. Exogenous xylitol can be metabolized in large quantities, intravenously 0.4 gm/kg/hour or 40 g/day orally raises the plasma level to a maximum of 1.5-16 mg/100 mL. The metabolic rate for xylitol is identical in both healthy and diabetic or uraemic patients and patients who suffered from liver diseases.|In /human/ studies with (14)C-xylitol 90% of C-atoms taken up could be recovered in products and intermediates of the glycolytic and pentose phosphate pathway.|For more Metabolism/Metabolites (Complete) data for Xylitol (8 total), please visit the HSDB record page.

No pharmacokinetic data available.|/In humans/ the initial fast distribution phase /for xylitol/ had a half life of about four minutes, while the apparent half life of elimination was approximately 20 minutes.|(14)C-xylitol disappeared extremely rapidly and the calculated half life is 165 seconds. ...|The half-life of exhalation of (14)CO2 after feeding with xylitol in unadapted /rats/ is 295 minutes, whereas rats which were adapted for 14 days to xylitol had a half-life of 237 minutes...|...Rats were administered (14)C-xylitol (250 mg) by intubation, the half-live of the resorption of xylitol was about 7 to 8 hr. The resorption rate is about 15-20% of that of glucose. After the animals had been fed xylitol for 14 days the half-life fell to 4.5 hr. ...

Xylitol is initially taken up by the microorganism and accumulates intracellularly. Accumulated xylitol is transported into an energy-consuming cycle, or the inducible fructose transport system. It is converted to non-metabolizable, toxic xylitol-5-phosphate via phosphoenolpyruvate: a constitutive fructose phosphotransferase system by _S. mutans_. This metabolic process of xylitol, without the gain of any energy molecules, results in the development of intracellular vacuoles and cell membrane degradation. _S. mutans_ dephosphorylates xylitol-5-phosphate and expels it from the cell, in which requires energy consumption. This ultimately leading to starving of microorganism and growth inhibition. Long-term exposure to xylitol can cause microorganisms to develop resistance to xylitol. This clinically beneficial selection process creates xylitol-resistant mutans strains that are less virulent and less cariogenic than their parent strains. Xylitol also increases the concentrations of ammonia and amino acids in plaque, thereby neutralizing plaque acids. A study suggests that xylitol may also promote remineralization of deeper layers of demineralized enamel by facilitating Ca2+ and phosphate movement and accessibility.

/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 if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the 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. /Poisons A and B/|/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 needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye 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 ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/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 as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ ... The tolerance of increasing amounts of dietary xylitol in 13 healthy children, aged seven to 16 years was investigated. Xylitol was administered as a supplement in addition to the children's regular diet. The daily dose was increased during successive 10-day periods from 10 to 25, 45, 65 and 80 grams. Gastrointestinal symptoms (flatulence, occasional abdominal pain and diarrhea) were recorded daily throughout the study. Prior to xylitol supplementation and after 20-50 days of dietary supplement serum uric acid and total cholesterol were measured. Flatulence was the most common side effect occurring relatively infrequently in almost every other subject during the 45 g/day intake, and in most subjects with greater frequency at the 80 g/day intake. Transient diarrhea occurred in four children on 65 g xylitol/day and in one child at 80 g/day. After 50 days of xylitol consumption, there was an increase in serum uric acid and cholesterol. However, the values were within the normal ranges for children.|/HUMAN EXPOSURE STUDIES/ During fructose, sorbitol, and xylitol perfusions, carbohydrate utilization was studied by continuous indirect calorimetry and compared with glucose utilization during pharmacologic inhibition of endogenous insulin secretion. The experiment was performed in 28 normal volunteers divided into 5 groups (glucose, fructose, sorbitol, xylitol, and saline), each subject being its own control. Insulin suppression was obtained by means of a constant infusion of epinephrine (6 ug/min) and propranolol (0.08 mg/min). After 90 min, during plasma insulin steady state, each sugar or polyol was infused at a rate of 6 mg/kg/min for 120 min. In contrast with a rise in plasma glucose from 161 +/- 6 mg/dL to 291 +/- 14 mg/dL during glucose infusion, glucose levels remained unchanged during infusion of the glucose substitutes. Carbohydrate oxidation showed a rise of 24, 65, 76, and 44 mg/min during infusions of glucose, fructose, sorbitol, and xylitol, respectively. Lipid oxidation rates decreased by 7, 20, 33, and 23 mg/min during the same infusions. These results indicate that fructose, sorbitol, and xylitol are oxidized at a higher rate than glucose during suppression of endogenous insulin secretion, without any significant rise in glycemia.|/HUMAN EXPOSURE STUDIES/ A study was carried out on nine subjects who had consumed xylitol for 4.8 to 5.3 years. During the years 1972-1974 these individuals consumed amounts ranging from 376-2520 mg/kg/day, and at the end of 1977, from 46 to 354 mg/kg/day. In 1978 the diets of these individuals were loaded with 82.3 to 1400 mg/kg/day (females 70 g/day, males 100 g/day) for 14 days using a strictly controlled diet, and subsequently for seven days while on a normal diet. During these periods and also during period of normal diet + sucrose loading, the following plasma and urinary parameters were measured. For serum; alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyltranspeptidase, lactate dehydrogenase, amylase: blood acid base balance. For urine; Uric acid, oxalic acid, 3-methoxy-4-hydroxymandelic acid, catecholamines (adrenalin, noradrenalin), metanephrines (m-o-methylnorepinephrine and m-o-methylnorepinephrine) urine: deposits, sediments and microcrystals, specific gravity, pH, U.V. and visible spectrum, volume; acid excretion in urine; urinary electrolytes; as well as the usual hematological, plasma and urinary parameters. There were no significant changes in any of the serum or urinary parameters measured.|/HUMAN EXPOSURE STUDIES/ Eighteen diabetic children received 30 g dietary xylitol during four weeks. A significant elevation of the uric acid concentration in serum was observed, also significant increases of total protein content and of inorganic phosphorus. In these children no diarrhea was noticed.|For more Human Toxicity Excerpts (Complete) data for Xylitol (21 total), please visit the HSDB record page.

Xylitol

Trade Names: Eutrit; Kannit; Klinit; Kylit; Newtol; Torch; Xyliton.

Ribitol: INACTIVE|Xylitol: ACTIVE|Table of percent relative sweetness and caloric values: [Table#7902]

... High-pressure liquid chromatography yields the most satisfactory results.

... High-pressure liquid chromatography yields the most satisfactory results.

Food additives|Human Drugs -> EU pediatric investigation plans|Human drugs -> Rare disease (orphan)|Food Additives -> HUMECTANT; SWEETENER; -> JECFA Functional Classes|Cosmetics -> Humectant; Skin conditioning

Food Additives -> HUMECTANT; SWEETENER;