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Color reaction of sugars with cysteine. II. Pigment formation from sugars and biological materials.

Among carbohydrates, D-glucose, D-mannose, D-galactose, and glycogen yielded a previously described fluorescent pigment, reddish in alkaline medium and yellowish in acid, when heated with L-cysteine in hydrochloric acid solution. D-Fructose and some pentoses yielded other patients. Among tissue hydrolysates, liver, small intestine, brain, and spleen were found rich in the cysteine pigment but little or none was produced from skeletal muscle, blood, or urine. Among subfractions of rat liver cells, the microsomal fraction proved the richest source of the pigment in nmol/mg protein, though the total yield from the soluble fraction was comparable to that from the microsomal fraction. In the latter fraction, only ribosomal particles yielded the pigment; smooth membrane did not. The pigment yield from yeast was comparable to that from liver. Yield from Escherichia coli K-12 was about one-forth that from yeast.

Animals↗

Structural studies of asparagine-linked sugar chains of human ceruloplasmin. Structural characteristics of the triantennary complex type sugar chains of human plasma glycoproteins.

The structures of the oligosaccharides released from human ceruloplasmin by hydrazinolysis were studied by sequential exoglycosidase digestion in combination with methylation analysis and periodate oxidation. A molecule of ceruloplasmin was shown to have two biantennary oligosaccharides A-1 and one triantennary oligosaccharide A-2, the structures of which are shown below. (Formula see text) The abbreviations used are: NeuAc, N-acetylneuraminic acid; Gal, galactose; GlcNAc, N-acetylglucosamine; Man, mannose.

Asparagine↗

Coupling between Na+ and sugar for sugar transport in a few Indian teleosts.

Transepithelial transport of D-glucose and D-xylose depends on the sodium ions in the filling solution in the fishes Ophiocephalus punctatus (carnivorous) and Heteropneustes fossilis (omnivorous). Under low Na+ concentration, the rate of transport decreases, while an increase in concentration brings about a corresponding increase in the transport of these nutrients in both fishes. In most of the cases, at different Na+ concentrations significant differences is in the absorbed amount. Glucose transport is affected by Na+ more than the transport of xylose and regional variations occur in the transported amount.

Animals↗

Human erythrocyte sugar transport is incompatible with available carrier models.

GLUT1-mediated, passive D-glucose transport in human erythrocytes is asymmetric, Vmax and K(m)(app) for D-glucose uptake at 4 degrees C are 10-fold lower than Vmax and K(m)(app) for D-glucose export. Transport asymmetry is not observed for GLUT1-mediated 3-O-methylglucose transport in rat, rabbit, and avian erythrocytes and rat adipocytes where Vmax for sugar uptake and exit are identical. This suggests that transport asymmetry is either an intrinsic catalytic property of human GLUT1 or that factors present in human erythrocytes affect GLUT1-mediated sugar transport. In the present study we assess human erythrocyte sugar transport asymmetry by direct measurement of sugar transport rates and by analysis of the effects of intra- and extracellular sugars on cytochalasin B binding to the sugar export site. We also perform internal consistency tests to determine whether the measured, steady-state 3-O-methylglucose transport properties of human erythrocytes agree with those expected of two hypothetical models for protein-mediated sugar transport. The simple-carrier hypothesis describes a transporter that alternately exposes sugar import and sugar export pathways. The fixed-site carrier hypothesis describes a sugar transporter that simultaneously exposes sugar import and sugar export pathways. Steady-state 3-O-methylglucose transport in human erythrocytes at 4 degrees C is asymmetric. Vmax and K(m)(app) for sugar uptake are 10-fold lower than Vmax and K(m)(app) for sugar export. Phloretin-inhibitable cytochalasin B binding to intact red cells is unaffected by extracellular D-glucose but is competitively inhibited by intracellular D-glucose. This inhibition is reduced by 13% +/- 4% when saturating extracellular D-glucose levels are also present. Assuming transport is mediated by a simple-carrier and that cytochalasin B and intracellular D-glucose binding sites are mutually exclusive, the cytochalasin B binding data are explained only if transport is almost symmetric (Vmax exit = 1.4 Vmax entry). The cytochalasin B binding data are consistent with both symmetric and asymmetric fixed-site carriers. Analysis of 3-O-methylglucose, 2-deoxy-D-glucose, and D-glucose uptake in the presence of intracellular 3-O-methylglucose, demonstrates significant divergence in experimental and theoretical transport behaviors. We conclude either that human erythrocyte sugar transport is mediated by a carrier mechanism that is fundamentally different from those considered previously or that human erythrocyte-specific factors prevent accurate determination of GLUT1-mediated sugar translocation across the cell membrane. We suggest that GLUT1-mediated sugar transport in all cells is an intrinsically symmetric process but that intracellular sugar complexation in human red cells prevents accurate determination of transport rates.

3-O-Methylglucose↗

ATP-dependent substrate occlusion by the human erythrocyte sugar transporter.

Human erythrocyte sugar transport presents a functional complexity that is not explained by existing models for carrier-mediated transport. It has been suggested that net sugar uptake is the sum of three serial processes: sugar translocation, sugar interaction with an intracellular binding complex, and the release from this complex into bulk cytosol. The present study was carried out to identify the erythrocyte sugar binding complex, to determine whether sugar binding occurs inside or outside the cell, and to determine whether this binding complex is affected by cytosolic ATP or transporter quaternary structure. Sugar binding assays using cells and membrane protein fractions indicate that sugar binding to erythrocytes is quantitatively accounted for by sugar binding to the hexose transport protein, GluT1. Kinetic analysis of net sugar fluxes indicates that GluT1 sugar binding sites are cytoplasmic. Intracellular ATP increases GluT1 sugar binding capacity from 1 to 2 mol of 3-O-methylglucose/mol GluT1 and inhibits the release of bound sugar into cytosol. Reductant-mediated, tetrameric GluT1 dissociation into dimeric GluT1 is associated with the loss of ATP and 3-O-methylglucose binding. We propose that sugar uptake involves GluT1-mediated, extracellular sugar translocation into an ATP-dependent cage formed by GluT1 cytoplasmic domains. Caged or occluded sugar has three possible fates: (1) transport out of the cell (substrate cycling); (2) interaction with sugar binding sites within the cage, or (3) release into bulk cytosol. We show how this hypothesis can account for the complexity of erythrocyte sugar transport and its regulation by cytoplasmic ATP.

3-O-Methylglucose↗

[Sugar transport, metabolism, accumulation and their regulation in fruits].

Photosynthates transported into fruits are mainly in the form of sucrose in most fruit tree species; but sorbitol takes the place of sucrose in woody Rosaceae plants. The transport of sugars across the plasma membrane from apoplastic space into cells is mediated by sugar transporters. The fact that gene expression of sugar transporters is upregulated just before and during sugar accumulation suggests the participation of sugar transporters in sugar accumulation of fruit. The sucrose-metabolizing enzymes participate in four futile cycles that involve sugar transport between cytosol, vacuole, amyloplast and apoplast. The increase in SS (sucrose synthase) and SPS (sucrose phosphate synthase) activities and mRNA levels during maturation parallels the increase in sugar accumulation indicates that the sucrose-metabolizing enzymes have important roles on sugar accumulation in fruits. The prerequisite for rapid accumulation of sugar in fruit is restriction of hexose catabolism and promotion of its synthesis. In woody Rosaceae plants, the fact that sucrose metabolism is also quite active in fruit suggests that sorbitol and sucrose probably play similar roles in fruit development. Sugars as signal molecules regulate the expression of genes involved in sugar transport and metabolism. Sugar transport, metabolism and accumulation are also regulated by natural environmental factors and cultural practices. The increase in sugar content of tomato fruit in acid invertase gene antisense-inhibited plants provides promising prospect of genetic engineering as a potential effective technique in regulation of sugar accumulation in fruits. Thus, the sugar content of fruit is determined by both intrinsic and extrinsic factors. The future research works will be focused on elucidating the mechanism of sugar signal and other intrinsic signals as well as extrinsic signals including nutrients, plant hormones and physical factors on sugar transport, metabolism and accumulation and the interrelationship among them.

Biological Transport↗

The sugar-fat relationship revisited: differences in consumption between men and women of varying BMI.

OBJECTIVE: To assess the relationship of dietary fat and sugar consumption in men and women with different body mass indices (BMI). To determine the actual food sources for sugar intake, comparing differences between men and women across BMI groups. The effect of excluding individuals with low energy intakes (that is, invalid data) on these relationships was also incorporated in the analysis. SUBJECTS: Subjects for this analysis were those individuals who participated in the 1986-1987 Dietary and Nutrition Survey of British Adults (DNSBA). METHOD: In the DNSBA, dietary intake was assessed using seven-day weighed food records, providing estimates of dietary fat and sugar intake. From the DNSBA database food records, sources of sugar intake were classified into five sugar containing food groups (high fat sweet products, fruits, dairy products, sugar products (excluding soft drinks) and sugar products (including soft drinks)). BMI was calculated from the measurement of height and body weight. RESULT: A positive relationship between BMI and dietary fat intake was found for men, both when fat was expressed as a percentage of energy and in absolute terms (g/d). This relationship was only replicated for women when intake was expressed in absolute terms. A negative relationship was found between sugar intake (as a percentage of energy) and BMI in men, but not women. Expressing sugar consumption in absolute terms did not produce a statistically significant relationship with BMI for either men or women. In women the only sugar source associated with BMI was high fat sweet products (for example, cakes, biscuits, chocolate), where higher intakes were related to higher BMIs. The reverse relationship was found for men. In men, BMI was also negatively related to the intake of sugar products (for example, table sugar, preserves, sugar confectionery), both when soft drinks were included and excluded. The inclusion of low energy reporters (LER) in the analysis altered the relationships between nutrients and BMI, particularly among women. The association between overall fat intake (g/d) and BMI was weakened, while the negative relationship with sugar intake was strengthened. In the case of women, the inclusion of LER completely reversed the relationship between consumption of high fat sweet foods (cakes, biscuits, chocolate) and BMI (due to the reduced reporting of these products by obese women). Fewer alterations in the relationships between BMI and the sources of sugar consumed were observed in men than in women when LER were included in the analysis. CONCLUSION: The relationships between dietary fat, sugar and BMI are different in men and women, and are dependent on the inclusion of LER, particularly in women. The results suggest that among women the consumption of high fat sweet products may be a factor in understanding obesity. Furthermore, the observation of high consumption of these foods among obese women is consistent with measured preferences for these high fat sweet foods. The altered representation of the data created by LER appears to distort the relationship between sugar, fat and the degree of obesity in men and women.

Adult↗

Structures of the sugar chains of recombinant macrophage colony-stimulating factor produced in Chinese hamster ovary cells.

The structures of the N- and O-linked sugar chains of recombinant human macrophage colony-stimulating factor (rhM-CSF) from Chinese hamster ovary (CHO) cells were studied. rhM-CSF is a homodimeric glycoprotein. Sugar composition analysis revealed that rhM-CSF contained 4.1 mol N-acetylgalactosamine, 10.3 mol N-acetylglucosamine, 5.0 mol mannose, 10.0 mol galactose, 1.4 mol fucose, and 11.8 mol sialic acid per mol of the monomer. The N- and O-linked sugar chains liberated by hydrazinolysis were N-acetylated, and the reducing-end sugar residues were tagged with 2-aminopyridine. The pyridylamino (PA-) sugar chains thus obtained were purified by HPLC. The structures of the PA-sugar chains were analyzed by a combination of reversed-phase and size-fractionation HPLC, and exoglycosidase digestions, from which the structures of the rhM-CSF sugar chains were estimated to be as follows: monosialo biantennary sugar chain (9 mol%), monosialo fucosylbiantennary sugar chain (10 mol%), disialo biantennary sugar chain (30 mol%), disialo fucosylbiantennary sugar chain (28 mol%), disialo triantennary sugar chain (7 mol%), trisialo triantennary sugar chain (11 mol%), and trisialo fucosyltriantennary sugar chain (5 mol%) for the N-linked sugar chains, and asialo (27 mol%), monosialo (51 mol%), and disialo (22 mol%) Galbeta1-3GalNAc for the O-linked sugar chains. Sialic acid residues were linked to the N-linked sugar chains through an alpha2-3 linkage.

Animals↗

Effects of types of sugar on the stabilization of protein in the dried state.

The effects of various sugars on the structural stabilization of protein during freeze-drying were investigated. The degree of native structure of protein that was freeze-dried and rehumidified at constant relative humidities (RHs) was evaluated by measurement of the alpha-helix content by Fourier-transform infrared spectroscopy. Bovine serum albumin (BSA) and several types of sugars, including sucrose, trehalose, and dextrans, were used as a model protein and sugars, respectively. The glass transition temperature, T(g), for the amorphous sugar samples was measured by differential scanning calorimetry (DSC) to characterize the structural stability of sugars. The dependence of the alpha-helix content (C(alpha-helix)) of BSA on the sugar content (c(sugar)) could, in most cases, be represented by a Langmuir-type equation: C(alpha-helix) = K x (C(alpha-helix) (max) - C(alpha-helix) (0)) x c(sugar)/(1 + K x c(sugar)) + C(alpha-helix) (0), where K is a constant, indicating the ability of amorphous sugar matrix to embed protein, and C(alpha-helix) (0) and C(alpha-helix) (max) indicate the alpha-helix content in the absence of sugar and saturating levels of sugar, respectively. The preservation effects of the sugars could be characterized by K and C(alpha-helix) (max). Both K and C(alpha-helix) (max) values tended to be higher with decreasing T(g) values for the amorphous sugar, probably because an amorphous sugar matrix with lower T(g) values is structurally more flexible. The rehumidification of protein that was freeze-dried in the presence of sugar induced the refolding of protein structure, whereas the protein dried alone did not show any recovery of its native structure.

Calorimetry, Differential Scanning↗

Effect of carbohydrates attached to polystyrene on hepatocyte morphology on sugar-derivatized polystyrene matrices.

Sugar-carrying polymers have been utilized as artificial matrices for cell adhesion in tissue engineering. We have developed sugar-derivatized polystyrenes (PV-sugars) as artificial matrices, which control hepatocyte adhesion and hepatic function. Hepatocytes adhere to PV-sugar matrices in a receptor-mediated manner. In this study, we designed a new galactose-derivatized PV-sugar, poly-(6-O-p-vinylbenzyl-alpha-D-galactose) (PV6Gal) and evaluated the role of carbohydrate attached to polystyrene (PS) backbone in the morphological difference of hepatocyte cultured on PV-sugar matrices. Hepatocytes spread on monosaccharide-derivatized PV-sugars but not on disaccharide-derivatized PV-sugars. The actin filament remained aggregated in the central area of the cell body on disaccharide-derivatized PV-sugars. Hepatocyte cell bodies fully were spread on collagen, and the actin filament was almost completely reorganized. Hepatocyte spreading on monosaccharide-derivatized PV-sugars, however, was caused by protrusive cell-matrix contact like lamellipodia and the actin filament was not completely reorganized. This indicated that hepatocyte spreading on PV-sugar matrices was restricted compared with ECM-mediated cell spreading. In addition, typical spheroid formation of hepatocytes was promoted on disaccharide-derivatized PV-sugars compared with monosaccharide-derivatized PV-sugars. Although hepatocytes adhered with different affinities to PV-sugar matrices, hepatocyte morphology was not affected by the adhesion affinity. We suggest that the type of carbohydrate attached to the PS backbone governs the morphology of hepatocyte cultured on PV-sugar matrices.

Animals↗

Intravenous and intrapulmonary administration of honey solution to healthy sheep: effects on blood sugar, renal and liver function tests, bone marrow function, lipid profile, and carbon tetrachloride-induced liver injury.

Safety of intravenous (i.v.) or intrapulmonary administration of different concentrations of honey and their effects on blood sugar, renal and liver function tests, bone marrow function, lipid profile, and carbon tetrachloride (CCl(4))-induced liver damage were studied. Healthy sheep of either sex, 6-8 months old, were assigned randomly into the following groups: sheep received i.v. infusion of 5% honey in normal saline at 10-day intervals for 50 days and were compared with sheep that received 5% dextrose; sheep received higher doses of honey (50 g of honey) by i.v. infusion daily for 10 days; sheep received four higher doses of honey (80 g each dose) for 2 weeks; sheep received subcutaneous injection of CCl(4) after four doses of i.v. infusion of 80 g of honey, and estimations of serum gamma-glutamyl transpeptidase (SGGT), serum glutamic oxaloacetic transaminase (SGOT), and serum glutamate pyruvate transaminase (SGPT) were performed daily for 10 days postinjection; sheep received i.v. infusion of 40 g of honey, and blood sugar estimation was performed for 3 h at 30-min intervals after infusion and compared with sheep that received 5% dextrose; sheep received rapid i.v. injection of 40% honey or 40% dextrose, and blood sugar was estimated before and after injection; sheep received various concentrations of honey in distilled water (0.5 mL/1.5 mL, 0.75 mL/1.75 mL and 1.2 mL/2.2 mL), and blood sugar estimation was performed before and after inhalation. Results showed that i.v. or intrapulmonary administration of honey did not cause any adverse effect. Intravenous delivery of honey by slow infusion caused improvement of renal and hepatic function, bone marrow function, and lipid profile. It reduced SGOT, SGPT, triglyceride, cholesterol, blood urea nitrogen, and blood sugar and elevated serum protein, serum albumin, hemoglobin, white blood cell, and neutrophil percentage. Similar results were obtained with the use of higher doses of honey. CCl(4) caused mild elevation of SGPT and SGGT and lowering of SGOT in sheep that received repeated i.v. administration of honey before administration of CCl(4), whereas in control sheep CCl(4) caused significant elevation of all the liver enzymes. Intravenous infusion of 40 g of honey caused elevation of blood sugar for 90 min postinfusion, whereas it decreased blood sugar at 2 and 3 h postinfusion as compared with fasting blood sugar. Dextrose caused significant elevation of blood sugar at all time intervals. Similar results were obtained with the use of 10% dextrose or 80 g of honey. Addition of honey to dextrose caused less hyperglycemia as compared with dextrose alone. Acute injection of 20 mL of 40% dextrose significantly elevated blood sugar for 3 h postinjection, whereas little elevation in blood sugar was obtained after injection of 40% honey; the difference between honey and dextrose was significant. Inhalation of honey caused significant lowering of blood sugar during and after inhalation as compared with fasting blood sugar and water inhalation. The effect was greater with a higher concentration of inhaled honey. It might be concluded that slow i.v. infusion or rapid i.v. injection of honey in different concentrations was safe and could lower blood sugar and improve renal, hepatic, and bone marrow functions and lipid profile. Intravenous honey had a hepatoprotective effect against CCl(4)-induced liver injury. Inhaled honey was safe and reduced blood sugar significantly.

Administration, Inhalation↗

Regulation of GLUT1-mediated sugar transport by an antiport/uniport switch mechanism.

Avian erythrocyte sugar transport is stimulated during anoxia and during exposure to inhibitors of oxidative phosphorylation. This stimulation results from catalytic desuppression of the cell surface glucose transporter GLUT1 [Diamond, D., & Carruthers, A. (1993) J. Biol. Chem. 268, 6437-6444]. The present study was undertaken to investigate the mechanisms of GLUT1 suppression/desuppression. Sugar uniport (sugar uptake or exit in the absence of sugar at the opposite side of the membrane) is absent in normoxic avian erythrocytes, but sugar antiport (sugar uptake coupled to sugar exit) is present. Exposure to cyanide and/or to FCCP (mitochondrial inhibitors) stimulates erythrocyte sugar uniport but not sugar antiport. K(m)(app) for 3-O-methylglucose uniport and antiport are unaffected by metabolic poisoning. Ki(app) for inhibitions of 3-O-methylglucose uniport by cytochalasin B and forskolin (sugar export site ligands) are unaffected by progressive stimulation of sugar uniport. Cyanide and FCCP stimulation of 3-O-methylglucose uniport are associated with increased AMP-activated protein kinase activity. Purified human GLUT1 is not phosphorylated by exposure to cytosol extracted from poisoned avian erythrocytes. FCCP does not stimulate GLUT1-mediated 3-O-methylglucose uptake in K562 cells but does increase K562 AMP-activated protein kinase activity. FCCP stimulation of 3-O-methylglucose uniport in resealed erythrocyte ghosts requires cytosolic ATP and/or glutathione. The nonmetabolizable ATP analog AMP-PNP cannot be substituted for ATP in this action. These results are contrasted with allosteric regulation of human erythrocyte sugar transport and suggest that avian erythrocyte sugar transport suppression results from inhibition of carrier uniport function. Uniport suppression is not mediated by interaction with cytosolic molecular species that bind to the sugar export site. The antiport to uniport switch mechanism requires ATP hydrolysis, is associated with elevated AMP-activated kinase function, and, if triggered by this kinase, is mediated by factors absent in K562 cells and downstream from the kinase.

3-O-Methylglucose↗

Arsinothioyl-sugars produced by in vitro incubation of seaweed extract with liver cytosol analysed by HPLC coupled simultaneously to ES-MS and ICP-MS.

It has been shown, that in vitro incubation of Laminaria digitata extract (containing mainly As-sugar 1 (glycerol-arsenoribose) and As-sugar 3 (sulfonate-arsenoribose)) with liver cytosol, produced the same two arsenicals, as when L. digitata extract was treated with H(2)S. By parallel use of HPLC-ICP-MS and HPLC-ES-MS the compounds displayed mainly m/z 345 and m/z 409. A pure As-sugar 1 standard was obtained, and a standard of arsinothioyl-sugar 1 (m/z 345) was produced, by purging a solution of As-sugar 1 with gaseous H(2)S. The identity of arsinothioyl-sugar 1 was characterised by ES-MS, 1D and 2D NMR. Arsinothioyl-sugar 1 showed the same chromatographic behaviour and MS characteristics as one of the two arsenic-containing compounds (m/z 345) produced by incubation of L. digitata extracts with liver cytosol, and as the product of the incubation of As-sugar 1 with liver cytosol (HPLC-ICP-MS, HPLC-ES-MS). Assuming that As-sugar 3 reacts in a similar way to As-sugar 1 with H(2)S, it is most likely that the second unknown (m/z 409) is arsinothioyl-sugar 3. The degradation of As-sugar 1 in acidic solution (100 mM HCl) was followed by (1)H-NMR, and the relative slow degradation (t(1/2)= 17 h) suggests that arsenosugars are taken up from the stomach in their original chemical form, hence the study of arsenosugar incubation in tissue is highly relevant. The arsinothioyls are a new group of organoarsenicals, which have only recently been identified in nature. Here, arsinothioyl sugars are detected for the first time. The in vitro formation of arsinothioyl-sugars in liver cytosol suggests that arsinothioyls may be of large biochemical and toxicological importance.

Animals↗

Defining and interpreting intakes of sugars.

This paper clarifies the myriad of terminologies used to describe intakes of sugars by American consumers. In addition, it carefully critiques information sources used to explain and interpret consumption levels. Sugars are incorporated into foods for their biological, sensory, physical, and chemical properties. By chemical definition, the sugars normally consumed are the monosaccharides and disaccharides: glucose, fructose, galactose, sucrose, lactose, maltose, and trehalose. US governmental agencies use 4 terms to describe sugars: added sugars, caloric sweeteners, sugar, and sugars. Different sources are included when measuring sugars. Knowledge regarding intakes of sugars relies on food intake surveys (primarily dietary recalls) and economic food availability estimates. Although intake data may underestimate actual consumption, availability data tend to overestimate it. Furthermore, the sugars contents of many foods appearing in composition databases are derived from the summation of recipe ingredients rather than from actual measurements. Intakes of sugars over time (trends) must be viewed within the context of varying definitions, changes in food composition, changes in dietary intake methods, and acknowledged increases in the underreporting of intake. Agreement is needed to identify one common definition to describe intakes of sugars. Convergence between intake data and economic availability data would more accurately depict consumption. Precise amounts of sugars within currently available foods should be measured, not calculated. Without a common language, accurate and precise measurements, and consensus among scientists, educators, regulatory agencies, and the public, conversations regarding any health effects of sugars may lead to continued misunderstandings.

Adolescent↗

A comparative study of the word sugar and of its equivalents in Hindustani as traceable to Chinese.

Etymology enables words to deliver past facts and can become an independent source of knowledge. Here the word sugar is traced to the Chinese term Sha-Che, literally "Sand-Sugar plant," signifying a sand-like product from the sugar plant, which is sugar. Sha-Che underwent the following phonetic changes: Sha-Che = Sha-Ke = Shar-Ker = Sharkera, which became the Sanskrit word for sugar, with the variant Sha-Kera. Its popular vernacular form became Shak-Ker. This entered Arabic as Al-Shakker, changing into Al-Sukker, pronounced as "Assuker." Muslims in Spain gave the Spanish their word when Assuker = Azucar (Spanish). Sukker, the real Arabic word, entered Old French as Suker-e, Italian as Zuker-o or Zucckero, and German as Zucker. When "k" is emphasized it can become aspirated as "kh" or doubled as "kk," or mutate into "g." Sukker then changed into Sugar with the "s" further mutating into "sh," giving the final form Shugar, written as Sugar. The Greeks directly borrowed the popular vernacular word Shakker. It was Hellenized as Sakkharon, mentioned by Discoredes in 56 A.D. From the Greek it passed into Latin as Saccharum. In India the large crystalline form of sugar is called Misri. Its Chinese original is Mi-Sha-Li, "sweet-pebble-glassy," a sweet crystalline (glassy) substance the size of pebbles. Another form of sugar is in small crystals, which in a heap appear opaque-white or porcelain-white rather than transparent salt-white. Porcelain-white sugar was called Cheeni, where Cheeni = Porcelain. Thus, Cheeni does not mean Chinese sugar, nor Misri Egyptian sugar. Both these forms of sugar were sweetening agents not intended to be directly consumed. But a sweet, composed of sugar and an article of food, was known in Chinese as Kan-Di, "Sweet-Drop." This became Candy in English, Qand in Arabic, Khanda in Sanskrit and Khand in vernaculars.

Carbohydrates↗

[Estimation of radiation exposed area by the nuclear accident occurred at Tokai village using ESR measurements of household sugar].

The area of radiation exposure by the nuclear accident occurred at Tokai village in 1999 was estimated by the ESR measurement of 95 household sugar samples collected from the accident area. These samples were roughly classified into three types of sugar, fine white sugar, fine brown sugar and coarse brown sugar. The control fine white sugar showed no radical in the ESR spectrum, while those of fine brown sugar and coarse brown sugar showed the presence of a small amount of radicals. It was also shown that, among these three kinds of sugar, the radical concentration of fine white sugar sampled from wooden houses at the area similar to each other did not vary much with the samples, while those of fine brown sugar and coarse brown sugar varied to a considerable extent. Thus, the fine white sugar is considered to be more suitable for the estimation of the level of radiation exposure. The radical concentration of each fine white sugar sample was plotted against the distance from the site of the nuclear accident with a correction of the difference in the shielding effect between concrete houses and wooden houses. The samples obtained at more than 2 km north of the site of nuclear accident showed no ESR spectral signal to a detectable extent. On the other hand, the ESR spectra were observed from the samples obtained within 10 km south and 4 km west of the accident site. These results suggest that the radiation exposure by the contaminant blown by the northeast wind blowing on the day of the accident may occur at the south and west areas.

Electron Spin Resonance Spectroscopy↗