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PubMed1990

Influence of sialic acids on the galactose-recognizing receptor of rat peritoneal macrophages.

The interaction of the galactose-recognizing receptor from rat peritoneal macrophages with ligands containing terminal galactose residues, such as asialoorosomucoid, desialylated erythrocytes or lymphocytes, can be inhibited by free N-acetylneuraminic acid (Neu5Ac) and oligosaccharides or glycoproteins containing this sugar in terminal position. This effect of Neu5Ac on the receptor is specific. The other naturally occurring or most of synthetic neuraminic acid derivatives tested do not exhibit an equivalent inhibitory potency as Neu5Ac. Although free Neu5Ac inhibits 5-fold stronger (K50 = 0.2mM) than free galactose, clustering of Neu5Ac in oligosaccharides and glycoproteins does not lead to stronger inhibition, which is in contrast to galactose-containing ligands. A more branched (triantennary) sialooligosaccharide inhibits less than biantennary and unbranched sialooligosaccharides. This may be the reason, why complex sialic acid-containing ligands like native orosomucoid or blood cells are not bound and internalized by the macrophages. The dissociation of asialoorosomucoid from the receptor is slow under the influence of Neu5Ac and requires relatively high concentrations of this sugar, whereas the dissociation mediated by galactose is rapid and requires lower concentrations. An allosteric influence of Neu5Ac on the binding of galactose by the receptor is discussed.

Animals↗
PubMed1990

Coexistence of nerve conduction deficit with increased Na(+)-K(+)-ATPase activity in galactose-fed mice. Implications for polyol pathway and diabetic neuropathy.

We measured motor nerve conduction velocity (MNCV), Na(+)-K(+)-ATPase activity, polyol-pathway metabolites, and myo-inositol in sciatic nerves from control mice, galactose-fed (20% wt/wt diet) mice, and galactose-fed mice given the aldose reductase inhibitor ponalrestat (300-mg/kg diet). Treatments were maintained for 4 wk. Galactose feeding was associated with a 21.5% reduction in MNCV (P less than 0.001), which was almost completely prevented by ponalrestat. Galactose-fed mice showed an 81% increase in Na(+)-K(+)-ATPase (P less than 0.01), an effect completely prevented by aldose reductase inhibition. Treatment of a separate galactose-fed group with sorbinil (300 mg/kg diet) also attenuated the MNCV deficit and prevented the increased Na(+)-K(+)-ATPase activity associated with galactosemia. Accumulation of galactitol in the nerves of galactose-fed mice was prevented by aldose reductase inhibition, but there were no alterations in myo-inositol levels in the sciatic nerves of any group. These data show that exaggerated flux through the polyol pathway can cause an MNCV deficit that is unrelated to either myo-inositol levels or NA(+)-K(+)-ATPase activity.

Aldehyde Reductase↗
PubMed2000

A case-control study of galactose consumption and metabolism in relation to ovarian cancer.

Consumption or metabolism of dairy sugar and ovarian cancer have been linked based on evidence that galactose may be toxic to ovarian germ cells and that ovarian cancer is induced in animals by depletion of oocytes. We assessed consumption of dairy products and obtained blood for biochemical and molecular genetic assessment of galactose metabolism in 563 women with newly diagnosed epithelial ovarian cancer and 523 control women selected either by random digit dialing or through lists of residents in eastern Massachusetts and New Hampshire. We observed no significant differences between cases and controls in usual consumption of various types of dairy products or total daily lactose (the principal source of galactose in the diet); nor did we find that RBC activity of either galactose-1-phosphate uridyl transferase (GALT) or galactokinase differed. The mean (and SE) activity of uridine diphospho-galactose 4'-epimerase (in micromoles per hour per gram of hemoglobin) was, however, significantly lower (P < 0.005) in cases compared with controls, 20.32 (0.31) versus 21.64 (0.36). Ovarian cancer cases were also more likely to carry the N314D polymorphism of the GALT gene, generally predisposing to lower GALT activity. The difference was most evident for endometrioid and clear cell types of ovarian cancer, in which 3.9% of cases were found to be homozygous for N314D compared with 0.4% of controls, yielding an odds ratio and 95% confidence interval of 14.17 (2.62-76.60). We conclude that, whereas adult consumption of lactose carries no clear risk for the disease, certain genetic or biochemical features of galactose metabolism may influence disease risk for particular types of ovarian cancer.

Adenocarcinoma, Clear Cell↗
PubMed1998

[The experimental research of free calcium of the lens epithelial cells in galactose cataract].

OBJECTIVE: To study the changes of free calcium in the lens epithelial cells (LECs) of galactose cataract. METHODS: Wistar rats, 28 days old, were fed with 50% galactose forage to form cataract models. Then the concentration of free calcium of LECs was measured at the 1st, 3rd, 7th, 10th, 14th, 19th days after the galactose diet was given. RESULT: The concentrations of free calcium in LECs of galactose cataract increased apparently and reached the maximum at the 10th day after galactose diet. The maximum was 4 - 5 times higher than that of the normal group. CONCLUSION: The calcium concentration of LECs in galactose cataract increases but the degrees at different phases are not the same. The maximal concentration is at the phase when the cortex is opacified.

Animals↗
PubMed2003

Effect of curcumin on galactose-induced cataractogenesis in rats.

PURPOSE: Curcumin, the active principle of turmeric, has been shown to have both antioxidant and hypoglycemic activity in vitro and in vivo. The purpose of this study was to investigate the effect of curcumin on the onset and maturation of galactose induced cataract. METHODS: Sprague-Dawley rats (21 days old) were divided into 5 groups. The control group (A) received an AIN-93 diet, the galactose group (B) received 30% galactose in the diet, the test groups (C and D) received the B group diet plus 0.002% and 0.01% curcumin respectively, and group (E) received the control diet plus 0.01% curcumin, all for a period of 4 weeks. Cataract progression due to galactose feeding was monitored by slit lamp microscope and classified into 4 stages. At the end of the experiment biochemical parameters such as lipid peroxidation, aldose reductase (AR), sorbitol dehydrogenase (SDH), reduced glutathione, protein content, and protein carbonyls were measured in the lens. Advanced glycated end products (AGE) and protein oxidation were measured by AGE and tryptophon fluorescence respectively. Crystallin profile was analyzed by size exclusion chromatography (HPLC). RESULTS: Slit lamp microscope observations indicated that curcumin at 0.002% (group C) delayed the onset and maturation of cataract. In contrast even though there was a slight delay in the onset of cataract at the 0.01% level (group D), maturation of cataract was faster when compared to group B. Biochemical analysis showed that curcumin at the 0.002% level appeared to exert antioxidant and antiglycating effects, as it inhibited lipid peroxidation, AGE-fluorescence, and protein aggregation. Though the reasons for faster onset and maturation of cataract in group D rats was not clear, the data suggested that under hyperglycemic conditions higher levels of curcumin (0.01%) in the diet may increase oxidative stress, AGE formation, and protein aggregation. However, feeding of curcumin to normal rats up to a 0.01% level did not result in any changes in lens morphology or biochemical parameters. CONCLUSIONS: These results suggest that curcumin is effective against galactose-induced cataract only at very low amounts (0.002%) in the diet. On the other hand at and above a 0.01% level curcumin seems to not be beneficial under hyperglycemic conditions, at least with the model of galactose-cataract.

Aldehyde Reductase↗
PubMed1992

[Determination of galactose eliminating capacity after intravenous administration--a liver function test].

The authors discuss a simple method for assessment of the galactose elimination capacity after intravenous administration of a 20% solution, total dose 0.5 g galactose/kg body weight. In six blood venous samples after termination of an infusion (after 25, 30, 35, 40, 45 and 50 minutes) from an inserted venous catheter after assessment of the enzymatic estimation of the galactose concentration in individual samples the elimination line of galactose is assessed as well as its point of intersection (t) with the time axis. By means of these data along with the data on the amount of injected galactose and the amount of galactose excreted in the urine the galactose elimination capacity is calculated. The method is suitable for evaluation and monitoring of the functional state of the liver. It reflects the functional mass of liver parenchyma and is therefore a quantitative test of liver function.

Galactose↗
PubMed2006

[Study on cell senescence induced by D-galactose in cultured rat mesenchymal stem cells].

OBJECTIVE: To study morphological and biological senescence changes induced by D-galactose in the cultured rat mesenchymal stem cells. METHODS: After 3rd generations cultured in the DMEM-F12, MSCs were changed into DMEM-F12 medium containing 8 g/L D-galactose and cultured to the 6th generations as the inducement group. The comparison were the 6th generations which was cultured in the DMEM-F12 medium all along, and then identified by surface wave. Using flow cytometer to check the comparisons cell cycle change after swing in with 8 g/L D-galactose within the 4 days. In the first 7 days to draw the growth curve to the two groups. Optical and electronic microscope were used to identify the influences of characteristic morphological of mesenchymal stem cells of the two groups, the influences of biological markers were identified by single cell gel electrophoresis and beta-galactose dye. Results After treatment with D-galactose, the mesenchymal stem cells displayed morphological and biological changes in the cell senescence with the senescent characteristic morphological markers; 85% of the cells were X-gal dye masculine, and the signal cell gel electrophoresis showed DNA damnification. The flow cytometry showed that 90% of the cells stayed in G0/G1, but the cells in S and G2/M almost disappeared. However, the cells in the control group had no such DNA damages. CONCLUSION: D-galactose can induce senescence of the mesenchymal stem cells, and 8 g/L is the best concentration to do so. This study has provided a good model for the research of the mesenchymal stem cells senescence.

Animals↗
PubMed1991

Accurate prediction of death by serial determination of galactose elimination capacity in primary biliary cirrhosis: a comparison with the Mayo model.

We retrospectively analyzed the predictive accuracy of serial determinations of galactose elimination capacity in 61 patients with primary biliary cirrhosis. Death was predicted from the time that the regression line describing the decline in galactose elimination capacity vs. time intersected a value of 4 mg.min-1.kg-1. Thirty-one patients exhibited decreasing galactose elimination capacity; in 11 patients it remained stable and in 19 patients only one value was available. Among those patients with decreasing galactose elimination capacity, 10 died and three underwent liver transplantation; prediction of death was accurate to 7 +/- 19 mo. This criterion incorrectly predicted death in two patients with portal-vein thrombosis; otherwise, it did better than or as well as the Mayo clinic score. The latter was also tested on our patients and was found to adequately describe risk in yet another independent population of patients with primary biliary cirrhosis. Cox regression analysis selected only bilirubin and galactose elimination capacity, however, as independent predictors of death. We submit that serial determination of galactose elimination capacity in patients with primary biliary cirrhosis may be a useful adjunct to optimize the timing of liver transplantation and to evaluate new pharmacological treatment modalities of this disease.

Adult↗
PubMedDate not supplied

Determination of hepatic blood flow in the rat using sequential infusions of indocyanine green or galactose.

A method was developed for the estimation of hepatic blood flow in the rat using sequential infusions of one of two model substrates, indocyanine green or galactose. Either substrate was infused to steady state (achieved within 6 min of the start of indocyanine green infusion and within 40 min of the start of galactose infusion) through either the femoral or portal vein, and three steady state blood samples were obtained. Following a 30-min washout period, the same substrate was infused a second time through the alternate blood vessel. Using a pharmacokinetic approach, hepatic blood flow was estimated from the mean steady state concentrations during the two infusions and the infusion rate. The present method yielded hepatic blood flow estimates of 2.03 +/- 0.13 ml/min/g of liver (indocyanine green) and 2.28 +/- 0.49 ml/min/g of liver (galactose) in two groups of four adult male rats. A Monte-Carlo simulation experiment was conducted to assess the potential error introduced into the blood flow calculation by the moderate transhepatic extraction ratio of the two model substrates (0.386 +/- 0.049 for indocyanine green; 0.439 +/- 0.139 for galactose). The simulation experiment predicted calculational errors between 7.4% (indocyanine green) and 19.5% (galactose), based on the hepatic extraction ratio and the precision of the analytical method for the two compounds. The predicted errors were in good agreement with the variability in blood flow estimates observed experimentally (6.5% for indocyanine green; 21.4% for galactose). The steady state approach employed appears to be associated with superior reproducibility as compared to previously reported methods utilizing bolus dose administration of marker compounds and calculations based upon AUC estimates.

Animals↗
PubMed1989

[A study on the metabolism of galactose cataract using a 31P-NMR spectroscopy].

Using a 31P-NMR spectroscopy, we monitored the metabolic kinetics of energy organophosphate compound in rat lens during the process of generating galactose cataract. The most remarkable metabolic change in the earlier phase of galactose cataract formation was found in alpha-glycerophosphate. This increased significantly, as compared to controls, since the day 3 of giving feed containing 25% galactose. The high level lasted for up to three weeks, decrease followed by a gradual decrease and subsequently a significant decrease at five weeks. Adenosine triphosphate (ATP) showed a significant decrease in the galactose group compared to the controls from two weeks after beginning of the experiment and the decrease continued. Inorganic orthophosphate increased gradually in the galactose group as compared to the controls, the increase being of significance at one week reading a maximum at two weeks followed by a subsegment decrease. Our basic study suggests that 31P-NMR spectroscopy is a useful technique in lens of the metabolic kinetics, to noninvasively determine the pathophysiology of galactose cataract, which has been studied biochemically and histologically.

Animals↗
PubMedDate not supplied

Decreased galactose absorption in dumping after colon interposition.

Intestinal absorption was examined using an oral galactose test in colon interposition patients with dumping (no. 4) and without symptoms (no. 5). Normal subjects (no. 5), and patients after total gastrectomy (no. 7) and gastric resection (no. 4) served as controls. Galactose is absorbed in the same way as glucose, but does not stimulate insulin secretion. Colon interposition patients presented abnormally rapid postprandial transit and absorption for 20 minutes after the meal. After this rapid phase, colon interposition patients with dumping demonstrated a strong decrease in absorption rate, whereas the asymptomatic patients presented a normal rate during the whole follow-up period. The elimination of galactose from the blood was studied in eight patients after intravenous infusion of galactose; the disappearance was linear during 10 to 30 min after injection and did not explain the differences in blood galactose levels in the oral galactose test. We suggest a reactive reflux back to the intra-abdominal colon graft loop in the avagotonic intestinal tract as the mechanism for the differences in absorption. The most likely reason for this is the rapid initial phase transit through the coloantral anastomosis and pyloroplasty. To normalize postprandial transit and absorption as much as possible after colon interposition, a short intra-abdominal colon graft loop anastomosed to the posterior proximal stomach is suggested.

Colon↗
PubMedDate not supplied

[Elevated galactose transport into cells as the cause of development of hereditary galactosemia in rats].

A strain of rats with symptoms of inherited galactosemia (cataracts, hepatosplenomegaly, aminoaciduria etc) was produced by selection and inbreeding of Wistar rats highly susceptible to the galactosemic effect of galactose. The salient biochemical feature of these rats, like human galactosemics, is manifested as a decrease in the activity of galactose-I-phosphate uridyltransferase (Gal-I-PUT) in liver tissue and erythrocytes. However, the cross experiments have shown that the decrease in Gal-I-PUT activity was not required for expression of main galactosemia symptoms. Genetic analysis of cataract formation demonstrated that this trait was controlled by a single dominant gene. High transport rate of 14C-galactose into erythrocytes was a characteristic of galactosemic rats. Genetic analysis demonstrated that this trait was under the control of a single dominant gene, similar to the cataract formation. The intracellular accumulation of galactose ensured by its high transport, simultaneously with a decrease in Gal-I-PUT activity, were assumed to be the main reasons of galactosemic symptoms. The glucose transporter isolated from erythrocytes of the galactosemic rats, when integrated into the liposome membrane transferred more actively galactose into the liposomes than that of the control galactose resistant rats.

Animals↗
PubMed1986

Purification and characterization of a human lectin specific for penultimate galactose residues.

A novel lectin has been found in human plasma. The lectin was purified by affinity chromatography using an adsorbent in which 2-O-alpha-D-glucopyranosyl-O-beta-D-galactopyranosylhydroxylysine (Glc-Gal-Hyl) was coupled to Sepharose. The molecular weight of the lectin was determined by gradient gel electrophoresis to be approximately 240,000. On polyacrylamide gel electrophoresis in sodium dodecyl sulphate, the subunit had the molecular weight of 29,500. Composition analysis has shown the lectin is a glycoprotein in which 12% of the molecule consists of carbohydrate. Native human, horse, calf, sheep, rabbit, and rat erythrocytes were agglutinated by the lectin in the presence of calcium. Glc-Gal-Hyl, N-acetylated Glc-Gal-Hyl, and stachyose inhibited the hemagglutination, whereas monosaccharides, maltose, cellobiose, lactose, raffinose, galactosylhydroxylysine, and N-acetylated galactosylhydroxylysine were not inhibitory. The lectin is strongly inhibited by the desialylated bovine erythrocyte glycoprotein, which contains galactose beta 1-3galactose beta-sequence at the nonreducing termini of the sugar chains, whereas disialylated orosomucoid did not inhibit the lectin. These results indicate that the lectin recognizes the penultimate galactose residue in a hapten molecule in contrast to usual galactose-binding proteins or galactose-specific lectins, which recognize exposed, terminal galactose residues of sugar chains.

Amino Acids↗
PubMed1980

Sodium-potassium--dependent ATPase. II. Cytochemical localization during the reversal of galactose cataracts in rat.

The importance of enzyme Na-K-ATPase in the development of galactose-induced cataractogenesis is now well realized. In our recent studies we reported decreased level of activity of this enzyme with an increased duration of galactose feeding and the induced alterations in rat ocular lens. Our approach was to determine the level of Na-K-ATPase activity by ultrastructural cytochemical analysis of lenses and spectrophotometric analysis of the incubating media used for cytochemical localization as described by Ernst. Using these approaches, we have determined the activity level of this enzyme during the reversal phase of the galactose-induced injury to the lens. Our findings are presented in this report and show that the activity of Na-K-ATPase recovers rapidly and attains the normal level when the animals were transferred to Rat Chow diet after the establishment of mature cataracts resulting from galactose feeding. This study supports the previous biochemical and morphological findings that partial reversal of galactose-induced cataractous lens occurs upon discontinuation of feeding of cataractogenic agent galactose.

Animals↗
PubMed1983

[Effects of prolonged consumption of lactose or hydrolyzed lactose in the rat. 5. Intestinal metabolism of glucose and galactose].

Effect of Prolonged Consumption of Lactose or Hydrolyzed Lactose in Rats.--5. Intestinal Metabolism of Glucose and Galactose. The intestinal metabolism of galactose is different according to the form of ingestion. With a lactose diet (L), the galactose is abundant in intestinal contents (Tab. I), since neither the intestinal flora (Tab. II), nor the epithelial tissue (Tab. III) can easily metabolize the galactose. The glucose disappears more rapidly than the galactose (Tab. I). With a hydrolyzed lactose diet (LH), the intestinal contents of two hexoses are identical (Tab. I). In this case, the enzymic activity of epithelium metabolizes an amount of galactose 6 times as big as with the lactose diet (Tab. III).

Animals↗
PubMed1983

Effective liver blood flow: determination by galactose clearance.

Effective liver blood flow is the portion of total flow that perfuses functional sinusoids and is available for metabolic exchange. Clearance of galactose from blood at concentrations below 10 mg/dl (0.555 mmol/l) measures this index and is calculated during continuous infusion of 5% D-galactose at a rate of 50 mg/min. The low galactose concentrations are measured accurately by a new fluorometric assay, which gives a precision +/- 0.2 mg/dl (0.011 mmol/l). In healthy people, plasma galactose clearance was 1366 +/- 172 ml/min, and hepatic extraction was 95%. Clearance in cirrhotics depends on the stage of their disease: in a stable group of patients with advanced cirrhosis, clearance was 835 +/- 87 ml/min with hepatic extraction ranging from 60% to 95%. The day-to-day coefficient of variation was 4.5%. Direct comparison with flow-probe liver blood flow measured in 11 normal dogs showed that galactose clearance was not significantly different. These findings support the hypothesis that galactose clearance correlates with effective liver blood flow.

Animals↗
PubMed1995

Galactose-induced retinal microangiopathy in rats.

PURPOSE: The suitability of the galactose-fed rat as a model of diabetic retinopathy was examined in nondiabetic rats fed diets enriched with either 30% or 50% galactose for up to 2 years. METHODS: Retinal capillaries were examined by light and electron microscopy, and the prevalence or severity of diabetic-like lesions was quantitated. RESULTS: Histologic evaluation of trypsin digests of retina revealed significantly greater than normal frequencies of pericyte ghosts and acellular capillaries at both 15 and 23 months receiving a 50% galactose diet. Similar lesions were observed in rats receiving a 30% galactose diet for 23 months. Capillary basement membrane thickening, dilated hypercellular capillaries (or intra-retinal microvascular abnormalities), and foci of vascular cells appeared in rats fed 50% galactose, but saccular microaneurysms characteristic of retinopathy in diabetic patients, diabetic dogs, and experimentally galactosemic dogs were not observed. Administration of the aldose reductase inhibitor, Sorbinil, to rats fed 50% galactose resulted in a significant inhibition of cataract and of galactitol accumulation in nerve and blood (by more that 90%) and retina (by 62%), but did not inhibit development of the retinal microvascular lesions. CONCLUSIONS: Two years of galactosemia in rats seems to reproduce only a portion of the lesions characteristic of diabetic retinopathy in patients or dogs. Nevertheless, lesions characteristic of at least the early stages of retinopathy clearly do develop in this galactosemic rat model, and are not restrained by inhibition of retinal polyol accumulation by 62%.

Aldehyde Reductase↗
PubMed1993

Determination of galactose elimination capacity after intravenous administration in patients with chronic liver diseases.

The authors describe a simple method of examination of galactose elimination capacity after intravenous administration of a twenty per cent solution in the total dose of 0.5 g galactose/kg body weight. After enzymatic determination of galactose concentration in six samples of venous blood (taken within 25, 30, 35, 40, 45 and 50 minutes after finishing the galactose infusion) the elimination curve of galactose and the intersection point with the time axis (t) is assessed and the galactose elimination capacity is calculated. In patients with liver steatosis and steatofibrosis, chronic hepatitis and liver cirrhosis the mean values of galactose elimination capacity were significantly lower in comparison with healthy volunteers. The method is sufficiently reliable, precise and quickly performable. It is suitable for evaluation and monitoring of the functional liver capacity, severity and progression rate of liver diseases. (Tab. 1. Fig. 2. Ref. 28).

Chronic Disease↗