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.
分解：
Since xylitol is not utilized by most microoragnisms, products made with xylitol are usually safe from fermentation and microbial spoilage.
碰撞截面：
136.3 Ų [M+Na]+ [CCS Type: DT, Method: single field calibrated with Agilent tune mix (Agilent)]
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.
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.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
吸收
木糖醇通过被动扩散在小肠中被吸收，吸收速度较慢。
Xylitol is absorbed in the small intestine via passive diffusion with a slow absorption rate.
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.
CATALYTIC PYROLYSIS OF SOLID BIOMASS AND RELATED BIOFUELS, AROMATIC, AND OLEFIN COMPOUNDS
申请人：Huber George W.
公开号：US20090227823A1
公开（公告）日：2009-09-10
This invention relates to compositions and methods for fluid hydrocarbon product, and more specifically, to compositions and methods for fluid hydrocarbon product via catalytic pyrolysis. Some embodiments relate to methods for the production of specific aromatic products (e.g., benzene, toluene, naphthalene, xylene, etc.) via catalytic pyrolysis. Some such methods may involve the use of a composition comprising a mixture of a solid hydrocarbonaceous material and a heterogeneous pyrolytic catalyst component. In some embodiments, the mixture may be pyrolyzed at high temperatures (e.g., between 500° C. and 1000° C.). The pyrolysis may be conducted for an amount of time at least partially sufficient for production of discrete, identifiable biofuel compounds. Some embodiments involve heating the mixture of catalyst and hydrocarbonaceous material at high rates (e.g., from about 50° C. per second to about 1000° C. per second). The methods described herein may also involve the use of specialized catalysts. For example, in some cases, zeolite catalysts may be used; optionally, the catalysts used herein may have high silica to alumina molar ratios. In some instances, the composition fed to the pyrolysis reactor may have a relatively high catalyst to hydrocarbonaceous material mass ratio (e.g., from about 5:1 to about 20:1).
Biocatalytic acylation of sugar alcohols by 3-(4-hydroxyphenyl)propionic acid
作者：R. Croitoru、F. Fiţigău、L.A.M. van den Broek、A.E. Frissen、C.M. Davidescu、C.G. Boeriu、F. Peter
DOI：10.1016/j.procbio.2012.06.015
日期：2012.12
Abstract Enzymatic synthesis of aromatic esters of four different sugar alcohols (xylitol, arabitol, mannitol, and sorbitol) with 3-(4-hydroxyphenyl)propionic acid was performed in organic solvent medium, using immobilized Candida antarctica lipase (Novozyme 435), and molecular sieves for control of the water content. The influence of reaction parameters on the conversion has been investigated, including
Abstract Fabrication technique is an important factor for development of catalysts. Titanium dioxide (TiO 2 ) is one of efficient photocatalysts. In this work, we firstly report the fabrication of TiO 2 nanoparticles by sol-microwave method with cetyltrimethylammonium bromide (CTAB) surfactant. Absence of surfactant, microwave treatment significantly reduced the cluster sizes of TiO 2 , but high aggregations
摘要 制备技术是催化剂发展的重要因素。二氧化钛（TiO 2 ）是一种高效的光催化剂。在这项工作中，我们首先报道了使用十六烷基三甲基溴化铵 (CTAB) 表面活性剂通过溶胶-微波法制备 TiO 2 纳米颗粒。在没有表面活性剂的情况下，微波处理显着降低了 TiO 2 的簇尺寸，但观察到了 TiO 2 颗粒的高度聚集。CTAB对TiO 2 的形貌、簇大小和介孔结构有很大影响。因此，溶胶-微波法合成的TiO 2 表面积从15.97增加到37.60 m 2 /g，0.108 M CTAB。通过葡萄糖转化生产高附加值化学品（葡萄糖酸、木糖醇、阿拉伯糖和甲酸）来测试 TiO 2 的光催化活性。发现表面积，TiO 2 的介孔结构和孔径是葡萄糖转化和产物分布的关键特性。从反应测试来看，0.108 M CTAB/MW-TiO 2 实现了最高的葡萄糖转化率（62.28%）。
Osmotic delivery system
申请人：——
公开号：US20030175346A1
公开（公告）日：2003-09-18
An osmotic pharmaceutical tablet is described which comprises a single-layer compressed core surrounded by a water permeable layer having a passageway. The single-layer core contains (i) a non-ripening drug having a solubility per dose less than about 1 mL
−1
, (ii) about 2.0% to about 20% by weight of a hydroxyethylcellulose having a weight-average, molecular weight from about 300,000 to about 2,000,000, and (iii) an osmagent.
