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PubMed2004

Dextran from Leuconostoc mesenteroides augments immunostimulatory effects by the introduction of phosphate groups.

The immunological effects of phosphorylated dextran (in which phosphate groups were chemically introduced) on murine splenocytes were examined. When dextran produced by Leuconostoc mesenteroides was phosphorylated by a reaction with polyphosphoric acid in formamide solution for 48 h, the degree of phosphorylation of dextran was maximal. The highest phosphorus content (1.7%, wt/wt) was observed in 40 kDa of dextran. The mitogenic response of murine splenocytes was enhanced by the phosphorylated dextran, but its activity was not related to its molecular weight. A strong response was detected at a concentration of 10 to 500 microg/ml, and the highest activity was obtained 48 h after stimulation. Phosphorylated dextran was characterized as a B-cell-specific mitogen. The expressions of CD86 on CD8alpha- CD11c- and CD8alpha- CD11c+ cells were augmented by phosphorylated dextran. The levels of mRNA expression of gamma interferon and interleukin-10 on murine splenocytes were also increased by the stimulation. These results demonstrate that dextran exerts immunostimulation by the introduction of phosphate groups.

Animals↗

PubMedDate not supplied

Experience with a large dose (500 mg) of intravenous iron dextran and iron saccharate in peritoneal dialysis patients.

OBJECTIVE: To compare efficacy in anemia correction and side effects of large doses of intravenous (IV) iron dextran and iron saccharate preparations in peritoneal dialysis (PD) patients. SETTING: Tertiary-care teaching hospital of University of Toronto. DESIGN: Retrospective analysis of 379 PD patients who attended PD clinics in past 5 years. Of these 379 patients, 62 were selected to receive IV iron based on ferrokinetic markers of iron deficiency, noncompliance to or ineffectiveness of oral iron, or increased erythropoietin (EPO) requirement. INTERVENTION: Sixty-one patients received two IV iron injections of 500 mg each, 1 week apart, 33 patients received iron dextran, 23 received iron saccharate, and 5 received both iron dextran and iron saccharate. One patient developed anaphylaxis to a test dose of iron dextran and was excluded from further therapy. Blood samples were collected before and 3 and 6 months after iron infusions. RESULTS: At 3 months, the group's average hemoglobin rose from 98.3+/-18.3 g/L to 110.6+/-16.4 g/L (p < 0.0001). Ferritin rose from 104.9+/-115.4 microg/L to 391.5+/-294.1 microg/L (p < 0.0001), and transferrin saturation from 0.17+/-0.07 to 0.26+/-0.19 (p < 0.0001). Erythropoietin requirements fell from 7278.7 IU/week to 5900 IU/week (p < 0.01). Five of the 34 patients who received iron dextran developed minor side effects and 1 patient had anaphylaxis to the test dose. Of the 23 patients who received iron saccharate, 1 had an anaphylactic reaction and 2 had transient chest pain, which subsided without therapy. Overall, there were more side effects with iron dextran (7.4% of injections) compared to the iron saccharate group (4.3% of injections), but this difference was statistically insignificant. Although statistically insignificant, there was an increase in the number of peritonitis episodes during the 6 months after IV iron infusion, especially with iron dextran, compared to the peritonitis episodes during the 6 months before iron infusions. CONCLUSION: Our study indicates that IV iron in PD patients is effective in restoring iron stores and in decreasing EPO requirements. One anaphylactic reaction occurred in each group. Our data suggest that as much caution be exercised with iron saccharate as with iron dextran. The slight trend toward increased peritonitis rates after iron infusions needs to be investigated in a larger group of patients.

Adult↗

PubMed1992

Iron dextran treatment in peritoneal dialysis patients on erythropoietin.

STUDY OBJECTIVE: To evaluate maintenance parenteral iron dextran in chronic peritoneal dialysis (PD) patients receiving erythropoietin (rHuEPO). DESIGN: Parenteral iron dextran was investigated in PD patients with poor response to rHuEPO and/or side effects of oral iron. SETTING: Tertiary-referral university hospital PATIENTS AND METHODS: Seven ESRD patients (five males and two females) were studied. A test dose of 25 mg iron dextran was given before starting a maintenance dose. Iron dextran 100 mg was given intramuscular weekly or biweekly. Six patients received rHuEPO and one patient was on decadurabolin. RESULTS: Hematocrits increased significantly (p < 0.01) from 29 +/- 2% to 38 +/- 2% and serum ferritin increased from 267 +/- 104 to 660 +/- 104 ng/dl after iron dextran. Serum albumin increased from 3.1 +/- 0.3 to 3.6 +/- 0.2 g/dl (p < 0.05). No patient developed an anaphylactic reaction or delayed reaction. Mean duration of parenteral iron dextran treatment was 7 +/- 1 months. Mean dose of erythropoietin was reduced significantly (p < 0.05) from 119 +/- 20 units/kg/week to 87 +/- 20 units/kg/week before and during fifth month of iron dextran therapy. CONCLUSIONS: Weekly/biweekly maintenance intramuscular iron dextran injection was effective and safe iron supplemental therapy in PD patients with poor response or side effects to oral iron.

Adult↗

PubMed1990

Functional protein-polysaccharide conjugate prepared by controlled dry-heating of ovalbumin-dextran mixtures.

A functional ovalbumin-dextran conjugate was prepared by dry-heated storage at 60 degrees C and 65% relative humidity for 3 weeks. The emulsifying properties of the ovalbumin-dextran conjugate were about three times higher than those of an ovalbumin-glucose conjugate. SDS-electrophoresis patterns showed that the ovalbumin-dextran conjugate obtained by dry-heating was not as polydispersed as that obtained by cyanogen bromide-activated dextran. The average molecular weight of the ovalbumin-dextran conjugate was about 200,000. The excellent emulsifying properties of ovalbumin-dextran conjugate were maintained even at pH 3 and were further improved at pH 10. In addition, the emulsifying properties of the ovalbumin-dextran conjugate were greatly enhanced by preheating the conjugate at 100 degrees C. Thus, it is suggested that an ovalbumin-dextran conjugate prepared by controlled dry-heating can be used as a macromolecular emulsifier for food applications.

Dextrans↗

PubMed1992

Equivalent eighteen-hour lung preservation with low-potassium dextran or Euro-Collins solution after prostaglandin E1 infusion.

Improved techniques of pulmonary preservation would help alleviate the critical shortage of donor organs in lung transplantation and would improve early graft function. A previous study demonstrated that cold pulmonary artery flush with low-potassium dextran solution was superior to Euro-Collins solution in preservation of canine lung allografts stored for 12 hours when no pulmonary vasodilator was used before donor lung flush. The present study was designed to determine whether donor pretreatment with prostaglandin E1 would affect the superiority of low-potassium dextran as a preservation solution. Prostaglandin E1 was infused (50 micrograms/min) in 12 donor dogs until potent vasodilation was demonstrated. Low-pressure pulmonary artery flush (50 ml/kg) with either Euro-Collins or low-potassium dextran solution (n = 6 for each group) was performed at 4 degrees C in a randomized, blinded fashion. Heart-lung blocks were extracted and stored at 4 degrees C for 18 hours before left lung allografting. Inflatable cuffs were placed around each pulmonary artery, allowing independent study of the native and transplanted lungs. All 12 recipient dogs survived the 3-day assessment period. Lungs flushed and stored in Euro-Collins or low-potassium dextran solution provided equivalent gas exchange function on day 0 (arterial oxygen tension: Euro-Collins 289 +/- 105 mm Hg versus low-potassium dextran 265 +/- 111 mm Hg; mean +/- standard error of the mean) and on day 3 (Euro-Collins 516 +/- 45 mm Hg versus low-potassium dextran 354 +/- 77 mm Hg; p = 0.10). Mean pulmonary artery pressures in the transplanted lung were not significantly different in the Euro-Collins and low-potassium dextran groups on day 0 (21.4 +/- 2 mm Hg versus 33.7 +/- 5 mm Hg, respectively; p = 0.09) or on day 3 (20.2 +/- 2.7 mm Hg versus 24.2 +/- 5.1 mm Hg, respectively; p = 0.50). We conclude that there was no advantage of low-potassium dextran over Euro-Collins as a flush solution in this 18-hour canine single lung allograft model in which prostaglandin E1 was administered before pulmonary artery flush.

Alprostadil↗

PubMed2004

Methyl-DEAE-dextran: a candidate biomaterial.

The full quaternisation of DEAE-dextran was successfully attempted and an application of the quaternised product was suggested. Commercial DEAE-dextran was reacted with iodomethane at 60 degrees C in the presence of NaOH. The raw product was purified by dialysis, during which the iodide ion was replaced by chloride. N-methylation and O-methylation resulted from the reaction. A second methylation step produced no further changes in the molecule. Alkalimetry indicated the absence of amino groups in the methylated polymer molecule, thus testifying to a complete quaternisation. N-acetylcysteine (AcCy) was neutralised with the polymer in the hydroxide form, thus obtaining the methyl DEAE-dextran salt of AcCy (Me-DEAE-dextran/AcCy), whereby an ophthalmic formulation for the treatment of the dry eye syndrome was prepared. For comparison, the neutral AcCy salt of commercial DEAE-dextran (DEAE-dextran/AcCy) was prepared. The AcCy content in Me-DEAE-dextran/AcCy was higher than in DEAE-dextran/AcCy (23 vs 13%), while the viscosity of a solution containing the salt concentration corresponding to the therapeutic AcCy concentration (4%w/v) was lower with the former compared to the latter salt (20.5 vs 23.9 mPa s). Both solutions were ipotonic (245 mOsm/kg), whereas the commercial Tirocular is strongly hypertonic (900 mOsm/kg) and irritant.

Acetylcysteine↗

PubMedDate not supplied

Dextran sulfate suppresses cell adhesion and cell cycle progression of melanoma cells.

We have reported that dextran sulfate is a possible candidate for an antimetastatic drug because it inhibits cell adhesion. It has been demonstrated that dextran sulfate can detach cancer cells adhering to the bottom of plastic flasks, and that the detached cells do not readhere or proliferate. In this study, we investigated the effects of dextran sulfate on cancer cells, focusing on cell cycle regulators as well as cell adhesion molecules. The effects of dextran sulfate on the cell cycle were examined by flow cytometry, and changes in gene expression caused by dextran sulfate were analyzed by cDNA microarray to identify changes in adhesion and cell cycle genes. By flow cytometry, treatment with dextran sulfate increased the percentage of cells in the G1/G0-phase, and decreased those in the S- and G2/M-phases. Analysis by cDNA microarray revealed decreased expression of several genes essential for progression of the G1- and S-phases. The expression of the adhesion factors involved in metastases was also suppressed. Furthermore, we confirmed these changes in the gene expression by Northern and Western blotting. Our results indicate that dextran sulfate suppresses cell adhesion and cell cycle progression, both of which are essential for metastasis, suggesting that dextran sulfate could be used as an antimetastatic agent.

Animals↗

PubMed1991

Resuscitation of hypovolemic sheep with hypertonic saline/Dextran: the role of Dextran.

We evaluated the role Dextran-70 plays in small volume resuscitation of hemorrhage using hypertonic saline dextran solutions. Sheep were hemorrhaged (1.5 to 2 liters) over 2 hr to an arterial pressure of 50 mm Hg and were then resuscitated with 100 ml of either 7.5% NaCl (HS/0% Dex) alone, 7.5% NaCl/6% Dextran-70 (HS/6% Dex), or 7.5% NaCl/24% Dextran-70 (HS/24% Dex). During hemorrhage cardiac output was reduced to 40-50% of baseline levels. The major effect of the added dextran was a greater initial increase and more sustained normalization of plasma volume and cardiac output. At 15 min post-infusion, plasma volume was expanded 17 +/- 2% with HS/0% Dex; 27 +/- 2% with HS/6% Dex; and 56 +/- 8% with HS/24% Dex. A dose response effect of the added dextran was also apparent in the post-resuscitation increases in arterial pressure and cardiac output. At 3 min post-infusion, both variables improved with all solutions, but baseline levels were reached and exceeded only in the HS/24% Dex. The increased cardiac output correlated significantly with the degree of vascular expansion. Regression and extrapolation of the post-resuscitation data of plasma volume expansion and increased cardiac output to no volume expansion suggests that the hypertonic saline also augments cardiac output by an additional mechanism independent of volume. Our data show that the addition of dextran to hypertonic saline can play an important role in small volume hypertonic resuscitation by improving both the initial cardiovascular response and the sustainment of that response. Higher concentrations of dextran than currently used in hypertonic formulations may make small volume resuscitation more efficacious.

Animals↗

PubMed1985

Antibody response of BALB/c mice to dextran B1355S: alterations in the expression of an idiotype associated with the depletion of idiotype-binding cells.

In this study, we established that BALB/c mice recognize and respond to the idiotype (M104E IdI) of a major dextran-specific clonotype within the BALB/c mouse repertoire. This idiotype recognition is established by demonstrating the presence of idiotype-binding cells and by the production of antibodies specific for the private M104E idiotype. To determine whether or not the idiotype-recognizing cells play a regulatory role during an immune response to dextran, the idiotype-binding cells were selectively removed either by panning or by radiation-induced killing. Two significant effects are observed when the depleted spleen cells are immunized with dextran. First, there is a substantial increase in the proportion of anti-dextran antibodies that are M104E IdI+. The second effect of the idiotype-specific cell depletion is the production of significant amounts of M104E IdI+ immunoglobulin molecules which do not bind dextran. The depletion experiments produced no alteration in the concentration of anti-dextran antibodies found in the serum or in the number of dextran-specific PFC in the spleen. The data indicate that idiotype-reactive cells can play a role in regulating the level of individual clonotype expression (i.e., the M104E clonotype), but that an alternative mechanism must exist for regulating the absolute amount of anti-dextran antibody produced after immunization.

Animals↗

PubMed1989

Variable region cDNA sequences and antigen binding specificity of mouse monoclonal antibodies to isomaltosyl oligosaccharides coupled to proteins. T-dependent analogues of alpha(1----6)dextran.

Four mouse hybridomas specific for alpha(1----6)dextran, 16.4.12E (IgA kappa, C57BL/6), 28.4.10A (IgM kappa, BALB/c), 35.8.2H (IgG1 kappa, BALB/c), and 36.1.2D (IgM kappa, BALB/c) were obtained by immunization with the T-dependent Ag isomaltohexaose or isomaltotriose coupled to keyhole limpet hemocyanin or to BSA. Immunochemical characterization of the hybridoma antibodies showed that 16.4.12E and 36.1.2D had cavity-type combining sites, recognizing the terminal non-reducing end of alpha(1----6)dextran, whereas 28.4.10A and 35.8.2H had groove-type sites, recognizing internal linear segments of the dextran. The V region cDNA of the H and L chains of the antibodies were cloned and sequenced. VH of 16.4.12E and VH of 36.1.2D belonged to the X24 and Q52 germ-line gene families, respectively. The VH and V kappa sequences of 16.4.12E and V kappa sequence of 36.1.2D were highly homologous to those of W3129, the only anti-alpha(1----6)dextran mAb with a cavity-type site thus far sequenced; 16.4.12E differed from W3129 in the D, JH, and J kappa. VH genes of 28.4.10A and 35.8.2H were homologous to those of several anti-alpha(1----6)dextrans with groove-type sites, but belonged to the J558 germ-line gene family, differed from the other J558 anti-alpha(1----6)dextrans, probably representing a different germ-line subfamily. The L chain sequence of 28.4.10A encoded by V kappa-Ars and J kappa 2 was almost identical to other groove-type anti-alpha(1----6)dextrans obtained by immunizing with the T-independent glycolipid Ag, stearyl-isomaltotetraose. Use of T-dependent Ag such as isomaltosyl oligosaccharide-protein conjugates provides an additional parameter for probing the fine structure of antibody combining sites and evaluating the V-gene repertoire of anti-alpha(1----6)dextrans.

Amino Acid Sequence↗

PubMed1989

Influence of dextran on blood clearance and organ distribution of radiolabelled E. coli and on survival in experimental E. coli septicemia.

Previous reports indicated impaired function of the reticuloendothelial system following administration of dextran. In the present experimental study, intravenous injection of Escherichia coli resulted in four deaths among 15 rats pretreated with i.v. dextran 70, but none in 15 controls (p less than 0.05). To evaluate the influence of dextran on bacterial clearance from blood and distribution in organs, 125I-labelled, heat-killed E. coli was injected 1 or 24 hours following i.v. injection of 1.0 ml sterile saline solution or 1.0 ml dextran 70. After both of these intervals, dextran resulted in significant (p less than 0.05) decrease of blood clearance compared with the controls. The organ distribution in counts/minute (cpm)/g tissue was compared in liver, spleen and lungs. Splenic uptake was reduced at both times following dextran administration, while there was increase in pulmonary uptake at 1 hour and in hepatic uptake at 24 hours post-dextran (p less than 0.005 and p less than 0.02, respectively). Evaluation of cpm/total organ weight showed no change after dextran injection, except for increased (p less than 0.05) pulmonary uptake after 1 hour.

Animals↗

PubMed1979

Effects of dextran 70 on factor VIII activity.

A case of apparent association of dextran 70 therapy with reduced factor VIII activity in a 24-year-old white woman with thrombotic thrombocytopenic purpura (TTP) is reported. Diagnosis of TTP was based on clinical and laboratory data consistent with transient neurological deficits, thrombocytopenia and hemolytic anemia. Intravenous dextran 70 (250 ml every 12 hours) and oral prednisone (80 mg daily) were given for TTP. Additional oral medications included codeine, Maalox and Tabron. When assay showed a factor VIII activity of 14% on the third day of dextran 70 administration, the drug was discontinued and oral administration of dipyridamole (100 mg four times daily) was begun. Factor VIII activity increased to 82% on day six. Dextran 70 (125 ml every 12 hours) was resumed on day seven following a splenectomy on the previous day. When factor VIII activity subsequently decreased from 75% to 29% within two days, dextran 70 was again discontinued and dipyridamole reinstituted at its earlier dosage. The patient's discharge medications included dipyridamole and 60 mg of prednisone daily (to be tapered). Reports of dextran 70-induced hemostatic defects involving platelets and factor VIII are reviewed. Dextran will form, with factors I and VIII, cryoprecipitates that may reduce the activity of factor VIII. It is suggested that patients receiving dextrans be monitored with partial thromboplastin times and, if available, with assays of factor VIII activity.

Adult↗

PubMed1982

Effect of dextran-70 on increased microvascular fluid and protein flux after thermal injury.

The effect of a colloid (dextran-70) infusion on increased microvascular fluid and protein flux after thermal injury was compared with that seen with a crystalloid infusion. Lymph flow (QL) and lymph/phasma (L/P) protein content were used to monitor microvascular fluid flux and protein permeability in the lung and in burned and nonburned soft tissues, namely, skin and subcutaneous tissue, for 72 h in 13 sheep given a 30% TBS full-thickness burn. Vascular pressures were maintained constant with dextran in saline or lactated Ringer's. Mean fluid requirements for dextran were one-half that for crystalloid during the 24-h resuscitation period. However, plasma proteins decreased by 50% with dextran compared to 30% with crystalloid. An increase of 2-2.5 fold in QL was seen during resuscitation in the lung and nonburned soft tissue with crystalloid while the L/P protein ratio decreased, indicating no change in protein permeability. This QL response was prevented during dextran infusion. A rebound increase in soft tissue QL occurred after discontinuation of dextran, probably as a result of the severe residual hypoproteinemia. Burn QL and L/P were markedly increased during the entire 72-h period, indicating increased permeability. Dextran infusion accentuated the QL response in the burn microcirculation. We conclude that dextran decreases edema in nonburned tissue, but appears to increase the protein loss from burn tissue.

Animals↗

PubMed1983

Hemodynamic, biochemical and morphological changes in the dextran and D-galactosamine-induced edemas in rats.

Dextran (600 mg/kg i.p.) and D-galactosamine (300 mg/kg s.c.)-induced edemas in the rat have been evaluated and compared on the basis of hemodynamic, biochemical and morphological investigations. The genesis of the edema induced by dextran was quicker (1-3 hr) than that induced by D-galactosamine. The edema index at the levels of the paws was higher in the dextran (10.5 +/- 0.6) than in the D-galactosamine (5.1 +/- 0.4)-induced edema. Furthermore, the dextran-induced edema was associated with marked hypotension and a decrease in the plasma protein levels. Bradycardia, decrease in the cardiac output and the coronary blood flow were observed in both the edemas. Blood flows to the brain, kidneys, lungs, spleen and paws were decreased only in the dextran-induced edema. It was interesting to note that the percentage distribution of the cardiac output in the paws was decreased in the dextran-induced edema only. PGE2 levels were increased, whereas the histamine levels were decreased in the paw-skin in both the edemas. These changes were relatively more marked in the dextran edema. The levels of PGF2 alpha remained unchanged. The above findings have been further supported by our morphological data where relatively more degranulation of the mast cells and that too at a shorter period, was observed in the dextran-induced edema. Different mechanisms for the genesis of these two kinds of edemas have been suggested.

Animals↗

PubMed1983

Adverse reactions to dextran in Sweden 1970-1979.

In a retrospective investigation of the period 1970-1979, 478 reports on cases of dextran-induced anaphylactoid/anaphylactic reactions (DIAR) were found. In 458 of these dextran was judged to be the causative agent. The number of units of dextran 40 and 70 used during this decade was 313 598 and 1 051 668, respectively. During the last five years, when reporting of severe adverse drug reactions was mandatory, the incidence of severe DIAR per unit administered was 0.013% for dextran 40 and 0.025% for dextran 70. The incidence of fatal DIAR was 0.003% and 0.004%, respectively. We found a male: female ratio of 1.5: 1 for all DIAR while for the most severe DIAR this ratio was 3: 1. The mean age of the patients was higher in severe than in mild DIAR. Allergic disease did not predispose for severe DIAR. Diabetes, cardiovascular and pulmonary diseases and chronic inflammation were more frequent among the patients who had suffered the most severe DIAR. 22 reactions were characterized by fever and/or shivering, and in 19 of these cases the reaction occurred after infusion of more than one unit of dextran. Severe DIAR occur after infusion of a few ml of dextran. Fatal DIAR during anaesthesia occurred almost exclusively in patients under spinal or epidural blockade. A favourable outcome of resuscitation in DIAR with cardiac arrest was possibly promoted by the infusion of large amounts of crystalloid fluids. We could not show that therapy with steroids, epinephrine or isoprenaline influenced the outcome. Fatal DIAR occurred even after infusion of only 0.5-1 ml of dextran, and we strongly advise against the use of "biological test-doses".

Aged↗

PubMed1984

[Heart arrest during dextran infusion despite hapten blockade].

In a running clinical prospective study on the incidence of adverse reactions to colloidal polysaccharides (randomised, single blind, n = 300) a bronchospasm followed by cardiac arrest occurred during dextran infusion although the necessary hapten blockage with monovalent dextran-1 had been effected. Resuscitation was successful. Directly after this, surgery was carried out as planned under general anaesthesia. The 69-year-old patient was discharged without noticeable sequelae. For the first time in the literature on dextran the studied sample allows a generalisation: The event occurred with an incidence of about 0.9% (of 116 patients who had received dextran infusion). This incidence corresponds to a confidence interval ranging from 0.02 to 4.96%. If the study would be continued as planned, the upper limit of this interval signals the probability of another case of severe intolerance. The diagnosis "dextran adverse reaction" can be made in this case by clinical symptoms. Since no previous or concomitant medication had been administered as provided in the protocol to confirm the diagnosis as an adverse reaction to dextran by determination of the titer of dextran antibodies prior to infusion is not required and it may be concluded that dextran was the causative agent.

Aged↗

PubMed1983

Characterization of a mutant of serotype g Streptococcus mutans strain 6715 lacking dextran-induced agglutination.

A spontaneous mutant of Streptococcus mutans 6715 (serotype g) defective in dextran-induced agglutination ability was isolated. The wild type strain and its mutant were termed as 6715-DP and 6715-DN, respectively. Both strains possessed serotype g antigen, and exerted similar sugar fermentation patterns. Strain 6715-DP was rapidly and strongly agglutinated upon addition of high molecular weight dextran, whereas the mutant strain 6715-DN was not. [14C]Dextran prepared from Leuconostoc mesenteroides dextransucrase and [14C]sucrose bound to fresh or lyophilized 6715-DP cells, but not to the mutant 6715-DN cells. However, both strains adhered to a glass surface in the presence of sucrose. Furthermore, heat-treated (100 degrees C, 10 min) cells of both strains bound cell-free glucosyltransferase, although dextran agglutination ability of strain 6715-DP was destroyed by this treatment, indicating that receptors for dextran and glucosyltransferase were different entities. Furthermore, serotype c, e, and f strains S. mutans did not agglutinate upon addition of dextran, nor did they bind [14C]dextran. However, all these strains and both 6715-DP and 6715-DN strains induced marked dental caries in SPF rats. It is concluded that dextran-induced agglutination ability is not a necessary condition for S. mutans to induce dental caries.

Agglutination↗

PubMedDate not supplied

[Anticomplement activity of native dextrans].

An anticomplementary activity of native dextrans of various structure was studied among the nine dextrans studied, eight polymers exhibited the anticomplementary activity of variable magnitude; only one dextran, containing 95% of 1--6 links and 2% of 1--2 links was unactive. The highest activity was exhibited by dextrans with high content of 1--2 links; lower activity was observed in dextrans, containing high amount of 1--3 links. The anticomplementary activity was not found in partially hydrolyzed dextrans, containing 90% and more links of the 1--6 type, with molecular weight of 2-10(6) daltons and lower. Polyaldehydes, obtained from these dextrans by oxidation with iodic acid, acquired the anticomplementary activity, comparable with the activity of native dextrans.

Animals↗