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PubMedDate not supplied

Protective effects of Chinese herbs on D-galactose-induced oxidative damage.

A mixture of traditional Chinese herbs ('FTDA') was found to improve several oxidation-related biomarkers in D-galactose-induced mimetic aging mice. FTDA consists of seven herbal components: Cuscutae Semen, Schisandrae Fructus, Dioscoreae Rhizoma, Lonicerae Flos, Nelumbinis Semen, Angelica Radix and Poria, and is routinely used for treating mice with D-galactose-induced oxidative damage. Measurements of antioxidant status, including superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant status (TAS) and malondialdehyde (MDA) were made on blood, brain and liver tissue collected from animals after 60 days of treatment with D-galactose subcutaneous injections. High-dose, medium-dose and control groups exhibited higher levels of SOD, GSH-Px and TAS in their blood, as well as lower levels of serum MDA activity, compared with the D-galactose group. In the liver, all three experimental and PBS groups demonstrated significant increases in SOD activity and a decrease in MDA activity. The MDA activity decreased in medium-dose, high-dose and PBS groups, while medium-dose and PBS groups demonstrated increased SOD activity compared with that seen in the brain. These results support the efficacy of FTDA in improving the antioxidant status of D-galactose-induced mimetic aging mice.

Animals↗
PubMed1986

The galactose-recognizing system of rat peritoneal macrophages. Receptor-mediated binding and uptake of glycoproteins.

Binding and phagocytosis of sialidase-treated cells by peritoneal macrophages is mediated by a galactose-specific receptor. So far, only cells or particles exposing terminal galactose residues were demonstrated to be ligands. We present results obtained with a newly developed radio-receptor assay, which proves both binding and uptake of glycoproteins mediated by the galactose-recognizing receptor of peritoneal macrophages. Requirement of Ca2+ for binding is used to distinguish between reversibly surface-bound and irreversibly internalized ligands. By using this approach, the uptake of the ligand is followed and its inhibition with phenylglyoxal and N-ethylmaleimide is demonstrated. Evidence was also obtained that internalization is followed by degradation of the ligand. Studies on the specificity show that only galactose is recognized but that the binding strength depends on the arrangement of galactose residues presented by the ligand.

Animals↗
PubMed1989

Sialic acid, galactose and fucose on the surface of Ehrlich ascites tumor cells grown in glucose-free medium in the presence of uridine.

1) The content and accessibility of terminal sialic acid and galactose residues as well as the incorporation of [3H]fucose into glycoconjugates were determined in 48-h cultures of Ehrlich ascites tumor cells in a glucose-free medium supplemented with uridine, a compound which can fulfil the necessary functions of glucose. 2) Sialic-acid residues accessible to sialidase cleavage were reduced from 695 +/- 80 nmol/10(9) cells (controls) to 284 +/- 22 nmol/10(9) cells (43% of controls). In situ labeling using periodate oxidation followed by sodium borotritiide reduction revealed a tritium incorporation of 47 +/- 11% that of controls (= 4.1 x 10(5) cpm/mg protein). 3) Labeling of galactose residues of 80-90% of that of controls was achieved after treatment of the cells with galactose oxidase/sodium borotritiide. A nearly six-fold enhancement of tritium incorporation into galactose of control cells was observed after sialidase/galactose oxidase treatment and sodium borotritiide reduction (1.5----8.8 x 10(5) cpm/mg protein); only a 3.6-fold increase (1.2 x 10(5)----4.3 x 10(5) cpm/mg protein) was found with glucose-free cultured cells. It is concluded that the galactose content of the cell surface is reduced to about 50% of controls. 4) The incorporation of tritium into acid-insoluble precipitate after 24 h incubation with [3H]fucose and the activity of the acid-soluble fraction were enhanced by about 85% as compared to controls. The pattern of inhibition by tunicamycin of [3H]fucose uptake and incorporation was the same in glucose-containing standard medium and in glucose-free uridine medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

A new method of blood galactose estimation for mass screening of galactosemia.

A new method for quantitative determination of galactose in blood by fluorescence of NADH was described. The assay system consisted of beta-galactose dehydrogenase, NAD, buffer and a denatured blood disc (3 mm diameter), and the reaction was carried out for 1 hr at 37 degrees C. Denaturation of hemoglobin was accomplished by exposing the blood disc to a vapor of formic acid in an air-tight container; this procedure completely eliminated false positive cases of galactosemia. This method can be applied in a wide range of galactose concentration from low (0 mg%) to high levels (200-1,000 mg%) with the accuracy of 8.0 +/- 0.3 mg% from a coefficient of variation of 3.5%. Semi-quantitative assay was also possible by using a spot test like Beutler's method. The galactose content in one disc paper (3 mm diameter) of blood containing 5 mg% galactose is approximately 0.1 micrograms. The newly developed method is satisfactorily applicable in neonatal mass screening and clinical cases.

False Positive Reactions↗
PubMed1978

Effects of ingestion of triglyceride or galactose on secretion of gastric inhibitory polypeptide and on responses to intravenous glucose in normal and diabetic subjects.

Responses of plasma immunoreactive gastric inhibitory polypeptide (IRGIP) to oral triglyceride or galactose were compared in normal and mildly diabetic (non-insulin-dependent) subjects. After triglyceride the responses of IRGIP were similar, but after galactose those of the diabetics were slightly exaggerated. Both stimuli evoked increments of plasma immunoreactive glucagon (IRG) in diabetics but not in normal subjects. Plasma immunoreactive insulin (IRI) did not change. In normal subjects given oral triglyceride or galactose followed by intravenous (I.V.) glucose the early-phase response of plasma IRI was enhanced and glucose tolerance improved. In the diabetics, oral triglyceride did not affect insulin release or glucose tolerance after I.V. glucose; oral galactose elicited a slight increase of insulin release without improving glucose tolerance. In the diabetics the rise of plasma IRG after ingestion of triglyceride or galactose was maintained after I.V. glucose. It is concluded that endogenous GIP is insulinotropic and that there is partial resistance to this action in diabetes. The results were compatible with feedback inhibition of GIP secretion by insulin and with the suggestion that the rise of plasma IRG associated with secretion of GIP in diabetics may be due to the glucagonotropic action of this peptide.

Administration, Oral↗
PubMed2006

Effects of topical administration of an aldose reductase inhibitor on cataract formation in dogs fed a diet high in galactose.

OBJECTIVE: To determine effects of a topical formulation of an aldose reductase inhibitor (ARI) on the development of sugar cataracts in dogs fed a diet high in galactose. Animals-Ten 6-month old Beagles. PROCEDURES: Dogs were fed a diet containing 30% galactose, and after 16 weeks, 6 dogs were treated topically with a proprietary ARI formulation and 4 dogs were treated with a placebo. Cataract formation was monitored by means of slit-lamp biomicroscopy and fundus photography. Dogs were euthanized after 10 weeks of treatment, and lenses were evaluated for degree of opacity, myo-inositol and galactitol concentrations, and concentration of the ARI. RESULTS: All dogs developed bilateral cortical opacities dense enough to result in a decrease in the tapetal reflex after being fed the galactose-containing diet for 16 weeks. Administration of the ARI arrested further development of cataract formation. In contrast, cataracts in the vehicle-treated dogs progressed over the 10-week period to the mature stage. Evaluation of the isolated lenses after 26 weeks of galactose feeding indicated that lenses from treated dogs were significantly less optically dense than lenses from control dogs. Lenticular myo-inositol concentration was significantly higher in the treated than in the control dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that topical application of a proprietary ARI formulation may arrest or reverse the development of sugar cataracts in dogs fed a diet high in galactose. This suggests that this ARI formulation may be beneficial in maintaining or improving functional vision in diabetic dogs with early lens opacities.

Administration, Topical↗
PubMed1985

Mitosis in the lens epithelium of the galactose-fed rat after prolactin treatment.

We have investigated the effect of the anterior pituitary hormone, prolactin, on mitosis in the lens epithelium of the galactose-fed rat. Our findings indicate that prolactin had a stimulatory effect on galactose-triggered mitosis within 24 hours after hormone administration. After three full days of galactose-feeding and daily prolactin injections, lens epithelia from prolactin treated rats had fewer mitoses than those from saline-injected controls. At the time when the number of mitoses had fallen to a subnormal level due to galactose-feeding (i.e., after 7 days), lenses of prolactin-treated animals exhibited less of a decrease in mitotic activity. Thus, it seems that prolactin modulates the mitotic response of lens epithelial cells when animals are on a galactose-rich diet. This modulation may be due, among other things, to a general acceleration of the cataractogenic process, mediated by the osmoregulatory action of prolactin.

Animals↗
PubMed1987

Anomeric preference in uptake of D-glucose and of D-galactose by rat lenses.

To determine the anomeric preference of uptake of D-glucose and of D-galactose by rat lenses, we crystallized alpha-, beta-D-[U-14C]glucose (720 microCi/mmol) and alpha-, beta-D-[U-14C]galactose (180 microCi/mmol) by our method and incubated them separately with rat lenses for 1 min, because of the short half-life of mutarotation of alpha-D-glucose (9.6 min) and of alpha-D-galactose (4.6 min) in HEPES medium at 30 degrees C. During aerobic incubation of rat lenses in HEPES medium containing radioactive alpha or beta anomer of D-glucose, there was no significant difference in the rate of uptake between alpha and beta anomers of D-glucose by rat lenses. However, 1.59 times greater incorporation of alpha-D-galactose was observed over that of beta-D-galactose under the same conditions.

Animals↗
PubMed1993

Elemental studies in rat lens during galactose cataract reversal.

Alterations in elemental composition of the normal lens have been reported to accompany galactose cataract development in rats. In this report we present the changes in regional distribution of Na, K, Cl, P, S and Ca during the reversal of galactose-induced cataracts. Elemental X-ray maps of lenses from young female Sprague Dawley rats fed 50% galactose for 20 days were examined at 0, 20, 40 and 90 days following the transfer of galactose fed rats to Purina Rat Chow diet. Reinstatement of normal elemental distribution accompanied the progression of lens transparency. By 90 days on the rat chow diet, K had increased and Na, Cl and Ca had decreased so that a near normal lenticular distribution of these elements was established. The reinstatement of elemental distribution during cataract reversal followed a pattern similar to that observed for alterations during cataract development, initiating near the equatorial surface and expanding centrally. The correlation between the alterations in the distribution of the elements studied and our previously reported morphological investigation of lenses during galactose cataract reversal is discussed in this report.

Animals↗
PubMed1979

Macrophage dependence of galactose oxidase induced transformation of human lymphocytes.

The role of macrophages in the transformation of human lymphocytes by the mitogen galactose oxidase was studied. Monocyte depleted, purified T or B cells did not undergo blastogenesis after treatment with galactose oxidase. When galactose oxidase-treated purified T cells were cultured with macrophages, a slight proliferative response was obtained. B cells treated similarly showed no response. When macrophages were treated with galactose oxidase, and then T & B, T, or B cells were added, proliferative responses were observed in all 3 categories. Finally, supernatants of media in which galactose oxidase-treated macrophages were cultured also demonstrated the property of stimulating lymphocyte transformation. These results are consistent with current concepts of mitogen "presentation" and the elaboration of soluble factors by macrophages in mediating the activation of lymphocytes in response to stimulating agents.

B-Lymphocytes↗
PubMed1982

Changes in intestinal galactose and leucine transport during development in the chick: effect of low external calcium.

There is some controversy in the literature as to the changes in sugar and amino acid absorption capacity by chicks during intestinal development in the posthatching period. For this reason, the transport of 5mM D-galactose and 4 mM L-leucine was studied in the mild intestine of the developing chick (range: 1 day to 35 days after hatch). In everted sacs, the net transepithelial transport of both substrates was maximal in the 1 to 3 days period and then it declined over the next 4 weeks. The final serosal:mucosal concentration ratio for galactose was 3.58 in 1 to 3-day-old chicks and fell to 1.62 in 26 to 30-day-old birds, while for leucine it fell from 3.52 to 1.50 in the same period. In intestinal rings from 1-day-old chicks, the uptake of 1 mM galactose after 1 min incubation was four times greater than in older animals. When the external calcium concentration was reduced from 2.5 mM (controls) to .1 mM the transport of galactose and leucine was markedly reduced: galactose transport was inhibited by 68 to 57% in 1 to 28-day-old chicks; leucine transport was inhibited by 82 to 50% in 1 to 7-day-old chicks with no significant effect thereafter.

Animals↗
PubMed1979

The effect of glibenclamide treatment on the insulin and glucagon responses to oral glucose and galactose in maturity onset diabetics.

Glibenclamide has been shown to stimulate an insulin releasing factor in the duodenum. The possibility that this effect is of importance in its hypoglycaemic action was investigated by studying the effect of galactose on insulin release before and after treatment with glibenclamide; galactose stimulates insulin release when given orally but has no effect when given parenterally; thus its ability to release insulin appears to reside in an action on a gut factor. Measurements of plasma glucose, insulin and glucagon were made on twelve maturity onset diabetic patients following an oral glucose tolerance test and an oral galactose tolerance test before and after one week of treatment with glibenclamide. Glibenclamide significantly reduced the blood glucose levels. Both basal insulin and basal glucagon levels were unchanged. The insulin response to oral glucose was enhanced. Glucagon levels before treatment did not suppression of glucagon levels. Galactose stimulated insulin release but insulin levels before and after treatment were identical. An effect of glibenclamide on gut insulin releasing activity was not demonstrated but the galactose tolerance test provides a useful technique by which to examine the enteroinsular axis.

Aged↗
PubMed1975

[Stimulation of DNA synthesis and mitoses in the rat liver in experimental galactosemia caused by the prolonged administration of galactose].

Feeding of rats with galactose-rich ration results in the activation of galactoso-1-phosphate-uridililtransferase in the liver after 2--4 days. By days 5--13, the activity of the enzyme decreased to the control level in spite of continued feeding of rats with galactose-rich ration. The activation of galactoso-1-phosphate-uridililtransferase occurred on the first 5 days of the experiment, whereas all proliferative activity in the liver increased from days 12--60, and the maximum mitotic was attained by the 20th and 50th days of feeding with galactose-rich diet. DNA synthesis also increased considerably, and this evidenced the increased H3-thymidine incorporation in hepatocyte nuclei. If one accept that the induction of enzyme transforming galactose to glucose is an adaptive response of cells (organism) to galactose in the diet, then the subsequent stage of adaptation would be hepatocyte proliferation.

Animals↗
PubMed1975

Galactose oxidase-induced blastogenesis of human lymphocytes and the effect of macrophages on the reaction.

Treatment of human lymphocytes with neuraminidase and galactose oxidase induced extensive blastogenesis. A less pronounced effect was observed after treatment of the cells with galactose oxidase alone. Macrophage-depleted human lymphocytes had a markedly reduced blastogenic response after treatment with neuraminidase and galactose oxidase. Incubation of the purified lymphocytes on macrophage monolayers markedly enhanced their response to neuraminidase and galactose oxidase. Furthermore, a stimulation of thymidine incorporation into purified untreated lymphocytes was noted after incubation of the cells on neuraminidase and galactose oxidase-treated macrophage monolayers.

Alcohol Oxidoreductases↗
PubMed2002

Effects of puerarin on D-galactose-induced memory deficits in mice.

AIM: To study the effects of puerarin on learning-memory behavior in aging mice induced by D-galactose and to explore in-brain mechanism of its effects. METHODS: The aging mice model were induced by sc D-galactose 0.12 g/kg daily for 6 weeks and meanwhile treated with three doses of puerarin once a day for 6 weeks. The spontaneous behavior and the learning-memory behavior were tested for the aging mice using open field and Y-maze on the day after the last treatment. Then the activity of superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) and lipofuscin in brain tissue were measured using UV-photospectrometer and fluorospectrophotometer analysis system. RESULTS: Compared with the D-galactose control group, puerarin 60 mg/kg was shown to increase significantly the spontaneous behavior and explorative response in the open field and improve remarkably the learning-memory ability of the aging mice induced by D-galactose. The percentage of memory retention increased from 69 %+/-9 % to 79 %+/-6 %. Puerarin 30 mg/kg and 60 mg/kg promoted remarkably the activity of SOD in the brain of the aging mice from (12.1+/-2.9) to (14.9+/-2.1) and(15.5+/-2.7) U/g wet brain weight, respectively, and decreased significantly the content of lipofuscin from (27+/-5) to (20+/-4) and (20+/-4) microg/g wet brain weight, respectively. CONCLUSION: Puerarin could improve the memory dysfunction produced by D-galactose. Improvement of the antioxidase activity of brain in the aging mice may be involved in this effect.

Animals↗
PubMed2002

[Effect of puerarin on learning-memory behavior and synaptic structure of hippocampus in the aging mice induced by D-galactose].

AIM: To study the effects of puerarin on learning-memory behavior of aging mice induced by D-galactose and its possible mechanism of action. METHODS: The aging mice were induced by s.c. 0.12 g.kg-1 D-galactose for 6 weeks. The aging mice were treated with three doses of puerarin once a day for 5 weeks. The spontaneous behavior and the learning memory behavior were tested in the aging mice using open field and Y-maze at the next day after the last treatment. The structure of Gray I synaptic interface in the CA3 area of the hippocampus was quantitatively analyzed by electronic microscope and computer image processing appliance. RESULTS: Compared with the D-galactose control group, puerarin (60 mg.kg-1) was shown to increase significantly the spontaneous behavior and explorative response in the open field, and improve remarkablely the learning and memory ability of the aging mice induced by D-galactose. Meanwhile, the thickness of post-synaptic density (PSD) was increased, and the width of the synaptic cleft in the hippocampus CA3 area was shortened. CONCLUSION: Puerarin showed an improvement effect against the memory impairment in the modelling aging-mice induced by D-galactose. A pathological alteration of synaptic interface structure in hippocampus of the mice may be involved in the effect.

Aging↗
PubMed1992

[The metabolism of galactose cataracts evaluated by phosphorous-31 nuclear magnetic resonance spectroscopy (2)].

The authors evaluated the metabolic kinetics of organophosphate compounds in the course of the evolution of galactose cataracts in rat lenses using phosphorous-31 nuclear magnetic resonance (31P-NMR) spectroscopy. Three-week-old rats (Lewis) were fed with a 25% galactose diet for three days, and one, two, three and four weeks. Metabolic changes in the lenses were measured and the following results were obtained: (1) Changes in glycerophosphorylcholine (GPC) levels over the time course were analogous to changes for choline phosphate (CP); both GPC and CP level showed a significant decrease in the galactose-fed sample compared with the controls from three days after ingestion, and then continued to decrease gradually. This suggested that the decrease of GPC was associated with the level of CP. (2) Inorganic orthophosphate (Pi) increased gradually after the ingestion of galactose, reaching a maximum at third week, and subsequently falling. Adenosine triphosphate (ATP) levels did not show any significant changes at one week, but had fallen significantly at two weeks. There might be metabolic pathways for production of ATP without requirement of Pi in the lens for at least the first one week. (3) Adenosine diphosphate (ADP) levels did not show any significant changes at three days, but had fallen significantly at one week. Nucleotide sugar (NS) increased gradually after the ingestion of galactose, reaching a maximum at second week, and then decreasing. This suggested that the ADP was converted to ADP sugar.

Animals↗
PubMed2005

[Protective effect of Danzhi-xiaoyao San on rat brain energy or material metabolism (correction of matebolism) dealt with D-galactose].

OBJECTIVE: To research the mechanism of Danzhi-xiaoyao San (DZXYS) for treating Alzheimer's disease model of rats dealt with D-galactose. METHOD: An Alzheimer's disease-like model of rats has been set up with sc. D-galactose 150.0 mg kg-1 D-1 x 49 d. Comparing with Acricept in 0.54 mg kg-1 D-1 dosage as a positive control drug, DZXYS in 12.636 g kg-1 D-1 x 49 d dosage has orally been administrated orally to treat the injury in the Alzheimer's disease-like model of rats. The energy charge in the cerebral tissues had been detested with waters liquid chromatography; the protein content and DNA content in the cerebral tissues had been detested with ultraviolet assay, the relative content of aldose reductase-mRNA is detested with RT-PCR. The difference was analyzed between the control rats without D-galactose, the model rats dealt with D-galactose, the model rats treated with Aricept and the model rats treated with DZXYS, it is significant as P<0.05. RESULT: 1) DZXYS can not affect the energy charge in their cerebral tissues. 2) DZXYS can increase the protein content from 0.3139 +/- 0.019468 to 0.3213 +/- 0.015528 (ni=10, P>0.05) in their cerebral tissues. 3) DZXYS can increase the total DNA content from 1.093 +/- 0.267 to 1.488 +/- 0.341 (ni=10, P<0.01) in their cerebral tissues. 4) DZXYS can increase the content of AR-mRNA in their cerebral tissue from 0.732 +/- 0.159 to 1.418 +/- 0.277 (ni=5, P<0.01). CONCLUSION: It suggests that DZXYS could be effective in human Alzheimer's disease for its stabling gene expression, maintaining protein characteristics, recovering signal transduction in the Alzheimer's disease-like model rats dealt with D-galactose.

Aldehyde Reductase↗