57-48-7 Usage
General Description
Different sources of media describe the General Description of 57-48-7 differently. You can refer to the following data:
1. D-Fructose is present as a monosaccharide in fruits and vegetables[1], as a disaccharide in sucrose (with D-glucose), and as oligoand polysaccharides (fructans) in many plants. It is also used as an added sweetener for food and drink, and as an excipient in pharmaceutical preparations, syrups, and solutions[2].
In equal amounts, it is sweeter than glucose or sucrose and is therefore commonly used as a bulk sweetener. An increase in high fructose corn syrup, as well as total fructose, consumption over the past 10 to 20 years has been linked to a rise in obesity and metabolic disorders[3]. This raises concerns regarding the short and long-term effects of fructose in humans.
Fructose is present more or less frequently than glucose in the juices of plants, fruits, and especially the honey, which is about half the solid matters[4]. It leads to an equal amount of glucose by the hydrolysis of sugar cane and a smaller proportion than some other less common sugars. It is used, such as glucose, in the production of glycogen. It enters the body through either be eaten as such or as the result of digestion of sugar cane. It is mainly changed into glycogen or triglycerides after reaching the liver, so do not enter largely in the blood circulation. Glucose and fructose are partially inter-convertible under the influence of very dilute alkali. It is not surprising; therefore, that fructose must be converted to glycogen in the liver, which on hydrolysis yields of glucose[5]. Dubois et al. reported that regular consumption of sugary drinks between meals increases risk of overweight among preschool children[6].
Fructose has been claimed to be of concern due to several factors: First, in the 1980’s, sucrose was replaced to a large extent, particularly in North America, by high fructose corn syrup (HFCS) in carbonated beverages. The intake of soft drinks containing HFCS has risen in parallel with the epidemic of obesity[7]. Second, dietary fructose has been implicated in risk factors for cardiovascular disease (CVD): 1. Plasma triglycerides (TG) and VLDL-TG increased following the ingestion of large quantities of fructose; 2. Fructose intake has been found to predict LDL particle size in overweight schoolchildren[8]. 3. A positive relationship has been demonstrated between fructose intake and uric acid levels[9]. Third, the use of fructose as a sweetener has increased. The third National Health Examination Survey (NHANES) demonstrated that over 10% of Americans’ daily calories were from fructose[10]. These studies suggest that the relationship between fructose and health needs re-evaluation.
2. Fructose is a monosaccharide. It is present in fruits and vegetables. Fructose is the major carbohydrate in the diet. It binds with glucose to form sucrose. Excessive intake of fructose is associated with obesity, type 2 diabetes and cardiovascular disease.
History of fructose consumption
Before the development of the sugar industry, free fructose was found in relatively few foods.[11] Relatively few unprocessed foods contain any significant amounts of free fructose monosaccharide. Historically, these foods have been relatively hard to obtain and they typically contain fructose in conjunction with glucose and/or fibre, which has significant implications for the absorption and metabolism of the former[12, 13]. As a consequence, humans have historically had low dietary fructose intakes[11]
Rise of fructose consumption
Fructose consumption has been escalating over the past several decades and is believed to play a role in the rising epidemic of metabolic disorders[14]. Fructose is a simple monosaccharide that occurs naturally in fruit, though the two main sources of dietary fructose in the Western diet are sucrose (table sugar) and high-fructose corn syrup (HFCS)[14]. Sucrose is cleaved enzymatically during digestion to produce one fructose molecule and one glucose molecule. HFCS, on the contrary, contains free fructose and glucose in varying ratios. A popular type of HFCS that is used to sweeten beverages in the United States – HFCS-55 – contains 55% fructose, 42% glucose and 3% oligosaccharides[15]. The 1999–2004 data from the National Health and Nutrition Examination Survey (NHANES) show that the average daily intake of fructose in the United States is now approximately 49 g, which equates to 9.1% of total energy intake[16]. In comparison, the average daily intake of fructose during 1977–1978 was 37 g[16]. The highest consumers of fructose are 19–22-year-olds, largely due to excess consumption of sugar-sweetened beverages. Fructose consumption as a percentage of total energy intakes amongst male and female 19–22-year-olds in the 95th percentile is 17.5 and 17.9%, respectively[16].
Source of fructose
It is located in fruits and honey. Main source is sucrose; the sucrose is hydrolyzed by sucrase into fructose and glucose. It is absorbed through facilitated diffusion and can be obtained from the portal blood to the liver where it is converted to glucose[17].
Biomedical importance of fructose
This disease occurs due to deficiency of aldolase B. It has been observed in children, when children receive fructose in the diet. The vomiting and hypoglycemia is an important feature of this disease. Fructose 1 phosphate accumulates in the liver. Accumulation exhausts inorganic phosphate thereby inhibiting both glycogen phosphorylase and the synthesis of ATP. Inhibition of these reactions leads to hypoglycaemia. AMP also accumulates and metabolism leads to increased production of uric acid leading to hyperuricemia and gout[18]. Treatment of this disease includes avoiding substances containing fructose[19].
Fructose metabolism
Sugar is present in fruits. Sucrose is hydrolyzed by sucrase to glucose and fructose. Dietary fructose is transferred from the intestine to the liver for metabolism. Fructose is converted to fructose 1 phosphate that further converted to acetone and glyceraldehyde dihydroxy, which is further converted to glyceraldehyde 3 phosphate to enter glycolysis. In the well-fed state, fructose is converted to glycogen[20] or triglycerides[21]. Hyperlipidemia, diabetes mellitus and obesity are interlinked. Consumption of fructose is increasing and is considered responsible for overweight. Several studies show that fructose increases incidence of obesity, dyslipidemia, insulin resistance, and hypertension. Metabolism of fructose takes place mainly in the liver and high fructose stream leads to accumulation of triglycerides in the liver (hepatic steatosis). This results in impairment of lipid metabolism and enhancement of expression of proinflammatory cytokine. Fructose alters glucose-induced expression of activated acetyl CoA carboxylase (ACC), pSer hormone sensitive lipase (pSerHSL) and adipose triglyceride lipase (ATGL) in HepG2 liver or primary liver cell cultures in vitro. This relates to the increased de novo synthesis of triglycerides in vitro and in vivo hepatic steatosis in fructose-fed versus glucose-and standard-diet mice fed. These studies provide new understanding of the mechanisms involved in fructose-mediated hepatic hypertriglyceridemia[22].
Rate of metabolism of fructose is more rapid than glucose, because triose formed from fructose 1-phosphate by pass phosphofructokinase, the primary rate-limiting step in glycolysis. Elevated levels of dietary fructose significantly elevate the rate of lipogenesis in the liver, because of the rapid production of acetyl-coenzyme A[23].
Fructose and diseases
Fructose and hyperuricemia
Increased intake of fructose is associated with hyperuricemia. Various studies indicate that that increased intake of sugar sweetened soft drinks and fructose is associated with risk of hyperuricemia in men[24].
Fructose and metabolic syndrome
It is hypothesized that fructose induces metabolic syndrome in health individuals. Study was carried out to investigate the role of uric acid in the hypertensive response. In this study, allopurinol was given to patients to lower the serum uric acid level. Ultimately it was found that excessive intake of fructose can increase the blood pressure and is responsible of metabolic syndrome but the lowering of serum uric acid level by allopurinol prevents the increase in mean arterial blood pressure[25].
Fructose and obesity
Fructose is almost similar to glucose because they are isomers to each other. Difference is in their metabolic pathway due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. In initial period when science was not so progressed, the diabetics patients were using fructose due to its low glycemic index. It has been observed now that obesity, diabetes mellitus, insulin resistance and hypertension are associated with chronic consumption of fructose. Dyslipidemia and impairment in hepatic insulin resistance are also due to increase intake of fructose in the diet. Adverse metabolic effects of fructose are responsible for hepatic de novo lipogenesis, hyperuricemia, oxidative stress and lipotoxicity. Epidemiological studies show that obesity, metabolic and cardiovascular disorders are also due to consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose). Adverse metabolic effects of fructose are usually on high consumption and there is lack of evidence of adverse effect on moderate consumption of fructose. Study shows that free fructose is more dangerous than consumption of fructose consumed with sucrose[26].
Fructose and hypertension
The rise in fructose intake has been paralleled by a rise in hypertension. A study of the US population during 2007–2008 found that 29% of adults were hypertensive, compared to 11–13% in 1939 and 24% during 1988–1994[27,28]. Epidemiological studies have hinted at a link between fructose consumption and hypertension. Jalal et al.[29] reported that excess dietary fructose (>74 g/day) in the form of added sugar was associated with higher blood pressure (BP) values in US adults who did not have a history of hypertension. Similarly, a study of 4867 adolescents found that SBP rose by 2mmHg from the lowest to the highest category of sugar-sweetened beverage intake[30]. In a prospective study of US adults, Chen et al.[31] found that drinking one less sugar-sweetened beverage per day was associated with a 1.8mmHg reduction in SBP and a 1.1mmHg reduction in DBP over 18 months.
References
Wang, Y.M.; van Eys, J. Nutritional significance of fructose and sugar alcohols. Annu. Rev. Nutr. 1981, 1, 437–475.
Hanover, L.M.; White, J.S. Manufacturing, composition, and applications of fructose. Am. J. Clin. Nutr. 1993, 58 (Suppl. S5), 724S–732S.
Bray GA, Nielsen SJ, Popkin BM: Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004, 79:537-543.
Ischayek JI, Kern M. US honeys varying in glucose and fructose content elicit similar glycemic indexes. J Am Diet Assoc 2006; 106(8):1260—2.
Faiq A. Carbohydrate metabolism. In: Biochemistry review. 1st ed. Karachi: Urdu Bazar; 2004. p. 1—100.
Dubois L, Farmer A, Girard M, Peterson K. J Am Diet Assoc 2007;107:924—34.
Bray G: How bad is fructose? Am J Clin Nutr 2007, 86:895-896 .
Aeberli I, Zimmermann MB, Molinari L, et al: Am J Clin Nutr 2007, 86:1174-1178.
Nakagawa T, Hu H, Zharikov S, et al: A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol Renal Physiol 2006, 290: F625-631.
Vos M, Kimmons J, Gillespie C, Welsh J, Blanck H: Medscape J Med 2008, 10(7):160.
Bray GA. How bad is fructose? Am J Clin Nutr 2007; 86: 895–6.
Lustig RH. Fructose: it’s ‘alcohol without the buzz’. Adv Nutr 2013; 4: 226–35.
Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 2010; 110: 1307–21.
Johnson RJ, Segal MS, Sautin Y, Nakagawa T, Feig DI, Kang D-H, et al. Am J Clin Nutr 2007; 86:899–906.
Hanover LM, White JS. Manufacturing, composition, and applications of fructose. Am J Clin Nutr 1993; 58:724S–732S.
Marriott BP, Cole N, Lee E. National estimates of dietary fructose intake increased from 1977 to 2004 in the United States. J Nutr 2009; 139:1228S–1235S.
Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr 1993;58(5):737—47.
Choi HK, Willett W, Curhan G. Fructose-rich beverages and risk of gout in women. J Am Med Assoc 2010;24304(20):2270—8.
Ali M, Rellos P, Cox TM. Hereditary fructose intolerance. J Med Genet 1998;35(5):353—565.
Segebarth C, Grivegnée AR, Longo R, Luyten PR, den Hollander JA. Biochimie 1991;73(1):105—8.
Angelopoulos TJ, Lowndes J, Zukley L, Melanson KJ, Nguyen V, Huffman A, et al. J Nutr 2009;139(6):1242—5.
Huang D, Dhawan T, Young S, Yong WH, Boros LG, Lipids Health Dis 2011;24:10—20.
Van der Meulen R, Makras L, Verbrugghe K, Adriany T, De Vuyst L. Appl Environ Microbiol 2006;72(2):1006—12.
Akram M. Management of acute gout. Inter J Fam Med 2010;3(4):233—4.
Perez S, Schold J. Int J Obes 2009;34:454—61.
Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev 2010;90(1): 23—46.
Egan BM, Zhao Y, Axon RN. Us trends in prevalence, awareness, treatment, and control of hypertension, 1988–2008. JAMA 2010; 303:2043–2050.
Robinson SC, Brucer M. Range of normal blood pressure. A statistical and clinical study of 11,383 persons. Arch Intern Med 1939; 64:409–444.
Jalal DI, Smits G, Johnson RJ, Chonchol M. J Am Soc Nephrol 2010; 21:1543–1549.
Nguyen S, Choi HK, Lustig RH, Hsu C-y. J Pediatr 2009;154:807–813.
Chen L, Caballero B, Mitchell DC, Loria C, Lin P-H, Champagne CM, et al. Circulation 2010; 121:2398–2406.
Chemical Properties
Different sources of media describe the Chemical Properties of 57-48-7 differently. You can refer to the following data:
1. White Cyrstalline Solid
2. Fructose occurs as odorless, colorless crystals or a white crystalline
powder with a very sweet taste.
Originator
Levugen,Baxter,US,1953
History
Despite this ubiquity, fructose remained a noncommercial product until the 1980s because of the expense involved in its isolation and the care required for its handling. The development of technologies for preparing fructose from glucose in the isomerized mixture led to a greater availability of pure, crystalline fructose in the 1970s. However, the price for pure fructose was high enough in 1981 that the product was not competitive with sucrose and corn syrups as a commercial sweetener. With the entry of corn wet-milling companies into the crystalline fructose market in the late 1980s, raw material economies and enlarged manufacturing scale led to a nearly 10-fold production increase within a five-year period, making fructose prices competitive with other sweeteners for specific applications.
Uses
Different sources of media describe the Uses of 57-48-7 differently. You can refer to the following data:
1. D-Fructose occurs in a large number of fruits, honey, and as the sole sugar in bull and human semen
2. fructose is a naturally occurring sugar in fruits and honey. It has moisture-binding and skin-softening properties.
3. Fructose is a sweetener that is a monosaccharide found naturally in fresh fruit and honey. It is obtained by the inversion of sucrose by means of the enzyme invertase and by the isomerization of corn syrup. It is 130–180 in sweetness range as compared to sucrose at 100 and is very water soluble. It is used in baked goods because it reacts with amino acids to produce a browning reaction. It is used as a nutritive sweetener in low-calorie beverages. It is also termed levulose and fruit sugar.
Production Methods
Fructose, a monosaccharide sugar, occurs naturally in honey and a
large number of fruits. It may be prepared from inulin, dextrose, or
sucrose by a number of methods. Commercially, fructose is mainly
manufactured by crystallization from high-fructose syrup derived
from hydrolyzed and isomerized cereal starch or cane and beet
sugar.
Definition
A sugar found in fruit juices,
honey, and cane sugar. It is a ketohexose,
existing in a pyranose form when free. In
combination (e.g. in sucrose) it exists in the
furanose form.
Manufacturing Process
200 gal of medium containing 2% sucrose, 2% corn steep liquor solids, 0.1%
potassium dihydrogen phosphate, and traces of mineral salts, was inoculated
with Leuconostoc mesenteroides NRRL B-512 and incubated at 25°C. During
growth, alkali was added automatically as needed to maintain the pH between
6.6 and 7.0. Fermentation was completed in 11 hours and the culture was
immediately adjusted to pH 5 to maintain enzyme stability. Bacterial cells
were removed by filtration and yielded a culture filtrate containing 40
dextransucrase units per ml, where one unit is the amount of dextransucrase
which will convert 1 mg of sucrose to dextran, as determined by the amount
of fructose liberated, measured as reducing power in 1 hour.
10 gal of the above culture filtrate was diluted to 40 gal with water, 33.3 lb of
sucrose was added to give a 10% solution, and toluene was added as a
preservative. Dextran synthesis was complete before 22 hours, and dextran
was harvested at 24 hours by the addition of alcohol to be 40% on a volume
basis.
The alcoholic supernatant liquor obtained was evaporated to recover the
alcohol and yielded a thick syrup, rich in fructose. Analysis showed the syrup
to contain 50.1% of reducing sugar, calculated as monosaccharide and to have
an optical rotation equivalent to 35.1% fructose. The percentages are
expressed on a weight/volume basis, and reducing power was determined by
the method of Somogyi, Jour. Biol. Chem. 160, 61 (1945). A portion (4.3
liters) of the syrup was cooled to 3°C. One-tenth of this volume was treated
by slow regular addition, with rapid stirring, of a 6-fold volume of cold 20%
calcium oxide suspension. A second portion was treated in the same manner,
and this process was continued until the entire volume of crude fructose syrup
had been utilized. The reaction mixture became thick with a white sediment
containing a profusion of microscopic needlelike crystals of calcium levulate.
Stirring was continued for 2 hours.The calcium levulate precipitate was separated from the reaction mixture by
filtration and washed with cold water. The precipitate was suspended in water
to give a thick slurry, and solid carbon dioxide added until the solution was
colorless to phenolphthalein. A heavy precipitate of calcium carbonate was
now present and free fructose remained in the solution. The calcium
carbonate precipitate was removed by filtration, and the filtered solution was
found to contain 1,436 g of fructose as determined by optical rotation. A small
amount of calcium bicarbonate was present as an impurity in solution and was
removed by the addition of oxalic acid solution until a test for both calcium
and oxalic acid was negative. The insoluble calcium oxalate precipitate was
removed by filtration.
The fructose solution was decolorized by treatment with activated charcoal
and concentrated under vacuum to a thick syrup. Two volumes of hot 95%
ethyl alcohol were added, and the solution was heated to a boil and filtered to remove a small amount of insoluble material. After cooling, three volumes of
ethyl ether were added, and the solution was allowed to stand overnight in
the refrigerator. Fructose separated from the solution as a thick syrup and was
separated from the supernatant liquid by decantation. The syrup was seeded
with fructose crystals and after standing in the cold for 4 days, became a
crystalline mass of fructose. The yield of dry fructose was 928 g. Additional
recoverable quantities of fructose are present in the crystallization mother
liquor. In continuous operation this mother liquor may be recycled for addition
to subsequent quantities of fructose syrup and the combined liquors
crystallized as in the foregoing example.
Therapeutic Function
Fluid replenisher, Pharmaceutic aid
Pharmaceutical Applications
Fructose is used in tablets, syrups, and solutions as a flavoring and
sweetening agent.
The sweetness-response profile of fructose is perceived in the
mouth more rapidly than that of sucrose and dextrose, which may
account for the ability of fructose to enhance syrup or tablet fruit
flavors and mask certain unpleasant vitamin or mineral ‘off-flavors’.
The increased solubility of fructose in comparison to sucrose is
advantageous in syrup or solution formulations that must be
refrigerated, since settling or crystallization of ingredients is
retarded. Similarly, the greater solubility and hygroscopicity of
fructose over sucrose and dextrose helps to avoid ‘cap-locking’
(sugar crystallization around the bottle cap) in elixir preparations.
Fructose also has greater solubility in ethanol (95%) and is
therefore used to sweeten alcoholic formulations.
The water activity of a sweetener influences product microbial
stability and freshness. Fructose has a lower water activity and a
higher osmotic pressure than sucrose. Syrup formulations may be
made at lower dry-substance levels than sugar syrups without
compromising shelf-life stability. It may be necessary to include a
thickener or gelling agent to match the texture or viscosity of the
sugar-equivalent formulation.
Fructose is sweeter than the sugar alcohols mannitol and
sorbitol, which are commonly used as tableting excipients.
Although fructose is effective at masking unpleasant flavors in
tablet formulations, tablets of satisfactory hardness and friability
can only be produced by direct compression if tablet presses are
operated at relatively slow speeds. However, by the combination of
crystalline fructose with tablet-grade sorbitol in a 3 : 1 ratio,
satisfactory direct-compression characteristics can be achieved. A
directly compressible grade of fructose, containing a small amount
of starch (Advantose FS 95, SPI Pharma) is also commercially
available. Pregranulation of fructose with 3.5% povidone also
produces a satisfactory tablet excipient.(1) The added sweetness of
fructose may also be used to advantage by coating the surface of
chewable tablets, lozenges, or medicinal gums with powdered
fructose.
The coprecipitation of fructose with hydrophobic drugs such as
digoxin has been shown to enhance the dissolution profile of such
drugs. Fructose apparently acts as a water-soluble carrier upon
coprecipitation, thereby allowing hydrophobic drugs to be more
readily wetted.
Biochem/physiol Actions
D-(?)-Fructose can enhance mood and gastrointestinal disturbances in fructose malabsorbers. It also possess metabolic and endocrine impact that shows that increased consumption of fructose is a contributing factor in the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome.
Safety
Although it is absorbed more slowly than dextrose from the
gastrointestinal tract, fructose is metabolized more rapidly. Metabolism
of fructose occurs mainly in the liver, where it is converted
partially to dextrose and the metabolites lactic acid and pyruvic
acid. Entry into the liver and subsequent phosphorylation is insulinindependent.
Further metabolism occurs by way of a variety of
metabolic pathways. In healthy and well regulated diabetics,
glycogenesis (glucose stored as glycogen) predominates.
Excessive oral fructose consumption (>75 g daily) in the absence
of dietary dextrose in any form (e.g. sucrose, starch, dextrin, etc.)
may cause malabsorption in susceptible individuals, which may
result in flatulence, abdominal pain, and diarrhea. Except in
patients with hereditary fructose intolerance, there is no
evidence to indicate that oral fructose intake at current levels is a
risk factor in any particular disease, other than dental caries.
storage
Fructose is hygroscopic and absorbs significant amounts of
moisture at relative humidities greater than 60%. Goods stored in
the original sealed packaging at temperatures below 25°C and a
relative humidity of less than 60% can be expected to retain stability
for at least 12 months.
Aqueous solutions are most stable at pH 3–4 and temperatures
of 4–70°C; they may be sterilized by autoclaving.
Purification Methods
Dissolve D(-)-fructose in an equal weight of water (charcoal, previously washed with water to remove any soluble material), filter and evaporate under reduced pressure at 45-50o to give a syrup containing 90% of fructose. After cooling to 40o, the syrup is seeded and kept at this temperature for 20-30hours with occasional stirring. The crystals are removed by centrifugation, washed with a small quantity of water and dried to constant weight under a vacuum over conc H2SO4. For higher purity, this material is recrystallised from 50% aqueous ethanol [Tsuzuki et al. J Am Chem Soc 72 1071 1950]. [Beilstein 31 H 321, 1 IV 4401.]
Incompatibilities
Incompatible with strong acids or alkalis, forming a brown
coloration. In the aldehyde form, fructose can react with amines,
amino acids, peptides, and proteins. Fructose may cause browning
of tablets containing amines.
Regulatory Status
Included in the FDA Inactive Ingredients Database (oral solutions,
syrup, and suspensions; rectal preparations; intravenous infusions).
Included in the Canadian List of Acceptable Non-medicinal
Ingredients.
Check Digit Verification of cas no
The CAS Registry Mumber 57-48-7 includes 5 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 2 digits, 5 and 7 respectively; the second part has 2 digits, 4 and 8 respectively.
Calculate Digit Verification of CAS Registry Number 57-48:
(4*5)+(3*7)+(2*4)+(1*8)=57
57 % 10 = 7
So 57-48-7 is a valid CAS Registry Number.
InChI:InChI=1/C6H12O6/c7-1-3-4(9)5(10)6(11,2-8)12-3/h3-5,7-11H,1-2H2/t3-,4-,5+,6?/m1/s1
57-48-7Relevant articles and documents
Photothermal strategy for the highly efficient conversion of glucose into lactic acid at low temperatures over a hybrid multifunctional multi-walled carbon nanotube/layered double hydroxide catalyst
Duo, Jia,Jin, Binbin,Jin, Fangming,Shi, Xiaoyu,Wang, Tianfu,Ye, Xin,Zhong, Heng
, p. 813 - 822 (2022/02/09)
The conversion of carbohydrates into lactic acid has attracted increasing attention owing to the broad applications of lactic acid. However, the current methods of thermochemical conversion commonly suffer from limited selectivity or the need for harsh conditions. Herein, a light-driven system of highly selective conversion of glucose into lactic acid at low temperatures was developed. By constructing a hybrid multifunctional multi-walled carbon nanotube/layered double hydroxide composite catalyst (CNT/LDHs), the highest lactic acid yield of 88.6% with 90.0% selectivity was achieved. The performance of CNT/LDHs for lactic acid production from glucose is attributed to the following factors: (i) CNTs generate a strong heating center under irradiation, providing heat for converting glucose into lactic acid; (ii) LDHs catalyze glucose isomerization, in which the photoinduced OVs (Lewis acid) in LDHs under irradiation further improve the catalytic activity; and (iii) in a heterogeneous-homogeneous synergistically catalytic system (LDHs-OH-), OH- ions are concentrated in LDHs, forming strong base sites to catalyze subsequent cascade reactions.
Sustainable production of 5-hydroxymethyl furfural from glucose for process integration with high fructose corn syrup infrastructure
Bajaj, Ishan,Chang, Hochan,Dumesic, James A.,Huber, George W.,Maravelias, Christos T.,Motagamwala, Ali Hussain,Somasundaram, Arun
, p. 3277 - 3288 (2021/05/25)
5-Hydroxymethyl furfural (HMF) is a platform chemical, which can be derived from lignocellulosic biomass, and used for production of liquid fuels and polymers. We demonstrate a process for production of HMF using sequential enzymatic and catalytic reactions of glucose to synthesize HMF, and simulated-moving-bed (SMB) separation to purify HMF. The adsorption thermodynamic parameters of glucose, fructose, and HMF on a commercial chromatography resin are experimentally determined for modeling the SMB-based HMF production process. The experimental data are used to develop a rigorous process model and then estimate the cost of production. Chromatographic separation of HMF has 16% lower operating costs compared to an extraction-based process and has a minimum selling price of approximately $1478 per ton. We demonstrate that the HMF process can be integrated with the high fructose corn syrup (HFCS) process, and we performed analyses considering two systems including construction of a new integrated facility and retrofitting an existing HFCS facility to produce HMF. Our analyses suggest that the latter approach is a promising short-term low-risk strategy to advance the HMF production technology to commercial scale.
Biochemical characterization of a recombinant acid phosphatase from Acinetobacter baumannii
Smiley-Moreno, Elizabeth,Smith, Douglas,Yu, Jieh-Juen,Cao, Phuong,Arulanandam, Bernard P.,Chambers, James P.
, (2021/06/09)
Genomic sequence analysis of Acinetobacter baumannii revealed the presence of a putative Acid Phosphatase (AcpA; EC 3.1.3.2). A plasmid construct was made, and recombinant protein (rAcpA) was expressed in E. coli. PAGE analysis (carried out under denaturing/ reducing conditions) of nickel-affinity purified protein revealed the presence of a nearhomogeneous band of approximately 37 kDa. The identity of the 37 kDa species was verified as rAcpA by proteomic analysis with a molecular mass of 34.6 kDa from the deduced sequence. The dependence of substrate hydrolysis on pH was broad with an optimum observed at 6.0. Kinetic analysis revealed relatively high affinity for PNPP (Km = 90 μM) with Vmax, kcat, and Kcat/Km values of 19.2 pmoles s-1, 4.80 s-1(calculated on the basis of 37 kDa), and 5.30 × 104 M-1s-1, respectively. Sensitivity to a variety of reagents, i.e., detergents, reducing, and chelating agents as well as classic acid phosphatase inhibitors was examined in addition to assessment of hydrolysis of a number of phosphorylated compounds. Removal of phosphate from different phosphorylated compounds is supportive of broad, i.e., 'nonspecific' substrate specificity; although, the enzyme appears to prefer phosphotyrosine and/or peptides containing phosphotyrosine in comparison to serine and threonine. Examination of the primary sequence indicated the absence of signature sequences characteristic of Type A, B, and C nonspecific bacterial acid phosphatases.
