Citrus Pectin and Oligofructose Improve Folate Status and Lower Serum Total Homocysteine in Rats

2003 ◽  
Vol 73 (6) ◽  
pp. 403-409 ◽  
Author(s):  
Thoma ◽  
Green ◽  
Ferguson
Keyword(s):  
Basal Diet ◽  
Sprague Dawley ◽  
Citrus Pectin ◽  
Deficient Diet ◽  
Sulfa Drug ◽  
High Fiber ◽  
Folate Status ◽  
Sprague Dawley Rats ◽  
Increased Risk ◽  
Total Homocysteine

Low folate status leads to increased total homocysteine (tHcy) concentration, and this has been associated with an increased risk of several diseases. Many colonic bacteria are capable of synthesizing folate, and certain dietary fibers may enhance this effect. We assessed the ability of non-fermentable (cellulose) and fermentable (citrus pectin and oligofructose) fibers to improve folate status and lower tHcy in rats. Weanling Sprague-Dawley rats were fed a folate-deficient diet with 5% cellulose for four weeks. Rats were then randomly assigned to one of five folate-adequate (400 mug/kg diet) test diets for 24 days. Diets were as follows: Basal; Basal + Sulfa Drug (succinylsulfathiazole); Cellulose; Citrus Pectin; and Oligofructose. High-fiber diets were formulated by diluting the basal diet such that the final diets contained 10% of the added fiber. Twenty-one days later, 3H-r-aminobenzoic acid was injected into the cecum, and rats were terminated three days later. Rats receiving the Citrus Pectin diet had significantly higher plasma (p = 0.011), erythrocyte (p = 0.035), and colonic tissue folate concentrations (p = 0.013) and lower tHcy (p = 0.003) than rats given the Cellulose diet. Rats receiving the Oligofructose had significantly higher plasma folate (p < 0.001) and lower tHcy (p = 0.032) concentrations than rats receiving the Cellulose diet. 3H-folate was detected in the livers of all rats except those receiving Sulfa Drug. Our study indicates that Citrus Pectin and Oligofructose, but not Cellulose, can significantly increase indices of folate status in rats and lower tHcy. It also confirms the ability of the large bowel to absorb folate.

Inhibition of 3'-Methyl-4-Dimethylaminoazobenzene-Induced Hepatocarcinogenesis by Portacaval Shunt

1978 ◽  
Vol 64 (2) ◽  
pp. 131-142 ◽  
Author(s):  
Silvio Fiala ◽  
Babulal Pragani ◽  
Melvin D. Reuber
Keyword(s):  
Large Dose ◽  
Gradual Increase ◽  
Portacaval Shunt ◽  
Basal Diet ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Glutamyl Transpeptidase ◽  
Functional Deficiency ◽  
Morphologic Changes ◽  
Intact Rats

Adult male Sprague Dawley rats on which end-to-side portacaval shunt (PCS) operation was performed did not develop hyperplastic nodules and hepatomas when they were fed 3'-methyl-4-dimethylaminoazobenzene in semisynthetic basal diet for periods of up to 169 days. In contrast, all the intact rats fed the same diet for only 75 days, developed hyperplastic nodules in the liver. Transferred to normal pellet for another 25 days, hepatomas developed in 100% of these animals. The amount of protein-bond 3'-Me-DAB was found to be much smaller in operated rats than in intact animals. The glutathione (GSH) level in PCS-operated rats was lower than in intact controls. A single large dose of 3'-Me-DAB led to the increase of only about 30% in the concentration of GSH during the period of 24–48 h, compared to the increase of 50–100% in non-operated rats. No clear tendency to a gradual increase in the activity of γ-glutamyl transpeptidase was noted in PCS-operated rats during the period of 5% months of 3'-Me-DAB feeding. The increase in GT-ase activity never exceeded 30% above the level of GT-ase in the livers of PCS-operated rats fed basal diet without the carcinogen. This striking inhibition of GT-ase increase induced by 3'-Me-DAB in PCS-operated rats contrasted with an increase of GT-ase activity by 5,000% found in livers of non-operated rats with hyperplastic nodules after 75 days of 3'-Me-DAB feeding and the increase by up to 10,000% in developed hepatomas. These effects and the inhibition of 3'-Me-DAB-induced hepatocarcinogenesis, manifested by lack of preneoplastic morphologic changes and the absence of hepatomas in rats after PCS, can best be explained by functional deficiency of the liver to metabolize the procarcinogen 3'-Me-DAB into an activated carcinogen.

scholarly journals Association between Chronic Acetaminophen Exposure and Allergic Rhinitis in a Rat Model

2015 ◽  
Vol 6 (3) ◽  
pp. ar.2015.6.0131 ◽  
Author(s):  
Nadieska Caballero ◽  
Kevin C. Welch ◽  
Patrick S. Carpenter ◽  
Swati Mehrotra ◽  
Tom F. O'Connell ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Mast Cells ◽  
Rat Model ◽  
Group Versus ◽  
Inferior Turbinate ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Increased Risk ◽  
Hematoxylin And Eosin

Background Several population studies demonstrated an increased risk of allergic rhinitis in patients exposed to acetaminophen. However, no histologic studies have been conducted to assess the relationship between acetaminophen exposure and allergic rhinitis. Objective In this study, we investigated the association between chronic acetaminophen exposure and the development of allergic rhinitis in a rat model. Methods Ten female Sprague-Dawley rats were randomly assigned to either a control (n = 5) or an acetaminophen group (n = 5). The acetaminophen group received 200 mg/kg/day of acetaminophen suspended in yogurt via oral gavage for 120 days. The control group received only the yogurt vehicle. Allergic behavioral responses, including nose rub, eye rub, ear scratching, and neck and/or face scratching, were quantified. The rats were killed, and the noses were harvested. The portion of the nose, including the nasal septum and the inferior turbinates, was embedded in paraffin, sectioned, and stained with hematoxylin and eosin to quantify the inflammatory infiltrate. Results The average number of allergic responses per animal was 13.2 in the acetaminophen group versus 6.2 in the control group (p = 0.032). All the rats in the acetaminophen group (100%) had mast cells infiltrating the lamina propria of the inferior turbinate, whereas mast cells were detected in only 40% of the animals in the control group. The average number of mast cells per animal in the acetaminophen group was 134 versus 21 in the control group (p = 0.048). Conclusions Our study was the first to demonstrate a histologic association between chronic exposure to acetaminophen and rhinitis. Further research to elucidate the mechanism that underlies these findings is necessary.

Effects of Dietary Carnosine and Vitamin E on Antioxidant and Oxidative Status of Rats

2008 ◽  
Vol 78 (45) ◽  
pp. 230-237 ◽  
Author(s):  
Wissam Ibrahim ◽  
Vickie Tatumi ◽  
Che-Chung Yeh ◽  
Chuen Bin Hong ◽  
Ching Kuang Chow
Keyword(s):  
Vitamin E ◽  
Antioxidant Status ◽  
Conjugated Dienes ◽  
Oxidative Status ◽  
Tocopheryl Acetate ◽  
Protein Carbonyls ◽  
Dietary Vitamin ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Sprague Dawley Rats

The purpose of this study was to determine if moderate levels of carnosine supplement, alone or in combination with vitamin E, enhance antioxidant status and/or provide protection against oxidative stress. Fiftyfour one-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet supplemented with either 0, 200, or 1000 mg L-carnosine, and either 0, 10, or 100 IU vitamin E (as all rec-α-tocopheryl acetate) per kg diet for 15 weeks. The antioxidant and oxidative status were assessed in the skeletal muscle, liver, and blood. Dietary vitamin E, but not carnosine, increased levels of vitamin E, decreased tissue peroxidizability, prevented incidence of myodegeneration, and reduced erythrocyte hemolytic stress. The levels of conjugated dienes, protein carbonyls, ascorbic acid, and nonprotein sulfhydryls, and activities of catalase, glutathione (GSH) peroxidase, and aldehyde dehydrogenase were not significantly altered by dietary carnosine or vitamin E. The results obtained suggest that supplementation of carnosine at levels of up to 1000 mg/kg diet does not significantly affect the antioxidant and oxidative status of rats.

scholarly journals Dietary Supplementation with Chitosan Oligosaccharides Alleviates Oxidative Stress in Rats Challenged with Hydrogen Peroxide

Animals ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 55 ◽  
Author(s):  
Ruixia Lan ◽  
Qingqing Chang ◽  
Lilong An ◽  
Zhihui Zhao
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Drinking Water ◽  
Dietary Supplementation ◽  
Basal Diet ◽  
Control Group ◽  
Sprague Dawley ◽  
Antioxidant Power ◽  
Chitosan Oligosaccharides ◽  
Sprague Dawley Rats

Oxidative stress is induced by excessive oxidative radicals, which directly react with biomolecules, and damage lipids, proteins and DNA, leading to cell or organ injury. Supplementation of antioxidants to animals can be an effective way to modulate the antioxidant system. Chitosan oligosaccharides (COS) are the degraded products of chitosan or chitin, which has strong antioxidant, anti-inflammatory, and immune-enhancing competency. Therefore, the current study was conducted to evaluate the hypothesis that dietary supplementation with COS alleviates the damage caused by oxidative stress in Sprague Dawley rats challenged with hydrogen peroxide (H2O2). The rats were randomly divided into three groups: CON, control group, in which rats were fed a basal diet with normal drinking water; AS, H2O2 group, in which rats were fed the basal diet and 0.1% H2O2 in the drinking water; ASC, AS + COS group, in which rats were fed the basal diet with 200 mg/kg COS, and with 0.1% H2O2 in the drinking water. In vitro, COS exhibited better radical scavenging capacity of 1, 1-diphenyl-2-picrylhydrazyl (DPPH), superoxide anion (O2−), H2O2, and ferric ion reducing antioxidant power (FRAP) than butylated hydroxy anisole (BHA). In vivo, dietary supplementation with COS alleviated the H2O2-induced oxidative damage, evidenced by comparatively increasing activity of SOD, CAT, GSH-Px, GSH, and T-AOC, and comparatively decreasing level of MDA in serum, liver, spleen, and kidney. COS also comparatively alleviated the H2O2-induced inflammation. In conclusion, COS supplementation reduced lipid peroxidation and restored antioxidant capacity in Sprague Dawley rats, which were challenged with H2O2.

Microvascular responses in copper-deficient rats

1989 ◽  
Vol 257 (5) ◽  
pp. H1607-H1612
Author(s):  
D. A. Schuschke ◽  
J. T. Saari ◽  
D. M. Ackermann ◽  
F. N. Miller
Keyword(s):  
Platelet Aggregation ◽  
Copper Deficiency ◽  
No Reduction ◽  
Fluorescein Isothiocyanate ◽  
Sprague Dawley ◽  
Cell Column ◽  
Deficient Diet ◽  
Endogenous Histamine ◽  
Sprague Dawley Rats ◽  
Platelet Aggregometry

In this study on copper deficiency, the rat crewmaster microcirculation was used as a model for endogenous histamine release and platelet thrombi formation. Male Sprague-Dawley rats were fed either a copper-supplemented diet (CuS, 5 ppm) or a copper-deficient diet (CuD, 0 ppm) for 5 wk before experimentation. The crewmasters of anesthetized rats were spread in a Krebs-filed tissue bath. In venules of CuS animals, photoactivation of intravascular fluorescein isothiocyanate tagged to bovine serum albumin caused significant platelet aggregation and reduction of red blood cell column diameter (RBCCD) by 40 min and stasis of flow by 60 min. In CuD animals there was only minor platelet aggregation and no reduction in RBCCD. Platelet aggregometry studies did not demonstrate reduced platelet aggregation in the CuD group, suggesting that copper deficiency alters the endothelium to inhibit adhesion. Compound 48/80 (1.0 and 10.0 microgram/ml) induced macromolecular leakage in both CuS and CuD groups, with the response in the CuD animals being significantly greater. The results demonstrate that copper deficiency results in alterations of the regulatory mechanisms governing inflammation and thrombosis.

Inulin/oligofructose and anticancer therapy

2002 ◽  
Vol 87 (S2) ◽  
pp. S283-S286 ◽  
Author(s):  
H. S. Taper ◽  
M. B. Roberfroid
Keyword(s):  
Cancer Treatment ◽  
Malignant Tumors ◽  
Lung Metastases ◽  
Human Cancer ◽  
Dietary Treatment ◽  
Basal Diet ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Interesting Approach ◽  
Cancer Risk Reduction

The results of our investigations indicate that dietary treatment with inulin or oligofructose incorporated in the basal diet for experimental animals: (i) reduced the incidence of mammary tumors induced in Sprague-Dawley rats by methylnitrosourea; (ii) inhibited the growth of transplantable malignant tumors in mice; and (iii) decreased the incidence of lung metastases of a malignant tumor implanted intramuscularily in mice. Moreover, besides such cancer risk reduction effects, the dietary treatment with inulin or oligofructose significantly potentiated the effects of subtherapeutic doses of six different cytotoxic drugs commonly utilized in human cancer treatment. If confirmed, such dietary treatment with inulin or oligofructose potentiating cancer therapy might become an interesting approach to complement classical protocols of human cancer treatment without any additional risk for the patients.

scholarly journals Sodium, potassium and chloride utilization by rats given various inorganic anions

1991 ◽  
Vol 66 (3) ◽  
pp. 523-532 ◽  
Author(s):  
Susan M. Kaup ◽  
Alison R. Behling ◽  
J. L. Greger
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Basal Diet ◽  
Renin Activity ◽  
Sprague Dawley ◽  
Sodium Potassium ◽  
Sprague Dawley Rats ◽  
Blood Pressures ◽  
Sodium And Potassium

The purpose of the present studies was to examine the effect of ingestion of sodium and potassium salts of various fixed anions on blood pressure, and to assess interactions among electrolytes. In the first study, Sprague-Dawley rats fed on purified diets supplemented with Na salts of chloride, sulphate, bisulphate, carbonate and bicarbonate for 7 weeks developed higher blood pressures than rats fed on the basal diet. In a second study, rats fed on Na or K salts of HSO4, HCO3 or Cl had higher blood pressures than rats fed on the basal diet. Blood pressure measurements were not correlated with plasma volume, plasma renin activity, or plasma atrial natriuretic peptide concentrations at 7 weeks. Plasma renin activity was depressed in rats fed on supplemental Na and even more in rats fed on supplemental K salts rather than the basal diet. Generally, rats fed on supplemental Na excreted Na in urine and absorbed Na in the gut more efficiently than rats fed on the basal diet or diets supplemented with K, but the anions fed also altered Na absorption and excretion. In a third study, rats fed on diets supplemented with any Cl salt, but especially KCI, absorbed K more efficiently than those fed on the basal diet. In studies 1 and 2, the efficiency of urinary excretion of K was greatest when HCO3 and CO3 salts were fed and least when HSO4 salts were fed. Despite large variations in the efficiency of absorption and excretion of Na and K, tissue levels of the electrolytes remained constant.

scholarly journals Changes in Bowel Microbiota Induced by Feeding Weanlings Resistant Starch Stimulate Transcriptomic and Physiological Responses

2012 ◽  
Vol 78 (18) ◽  
pp. 6656-6664 ◽  
Author(s):  
Wayne Young ◽  
Nicole C. Roy ◽  
Julian Lee ◽  
Blair Lawley ◽  
Don Otter ◽  
...  
Keyword(s):  
Resistant Starch ◽  
Physiological Responses ◽  
Basal Diet ◽  
16S Rrna Genes ◽  
Rrna Genes ◽  
Direct Result ◽  
Sprague Dawley ◽  
Content Type ◽  
Sprague Dawley Rats ◽  
Metabolite Profiles

ABSTRACTThe ability to predictably engineer the composition of bowel microbial communities (microbiota) using dietary components is important because of the reported associations of altered microbiota composition with medical conditions. In a synecological study, weanling conventional Sprague-Dawley rats (21 days old) were fed a basal diet (BD) or a diet supplemented with resistant starch (RS) at 5%, 2.5%, or 1.25% for 28 days. Pyrosequencing of 16S rRNA genes and temporal temperature gradient electrophoresis (TTGE) profiles in the colonic digesta showed that rats fed RS had altered microbiota compositions due to blooms ofBacteroidetesandActinobacteria. The altered microbiota was associated with changes in colonic short-chain fatty acid (SCFA) concentrations, colonic-tissue gene expression (Gsta2andEla1), and host physiology (serum metabolite profiles and colonic goblet cell numbers). Comparisons between germ-free and conventional rats showed that transcriptional and serum metabolite differences were mediated by the microbiota and were not the direct result of diet composition. Altered transcriptomic and physiological responses may reflect the young host's attempts to maintain homeostasis as a consequence of exposure to a new collection of bacteria and their associated biochemistry.

scholarly journals In Vivo Assessment of Zinc Deficiency on Craniofacial Growth in a Rat Model

2009 ◽  
Vol 03 (01) ◽  
pp. 10-15
Author(s):  
Cankat Kara ◽  
Recep Orbak ◽  
Ilhan Metin Dagsuyu ◽  
Zerrin Orbak ◽  
Necmettin Bilici ◽  
...  
Keyword(s):  
Soft Tissues ◽  
Atomic Absorption Spectrophotometry ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Zinc Intake ◽  
Group I ◽  
Sprague Dawley Rats ◽  
Group Ii ◽  
Rat Mandible

ABSTRACTObjectives: The aim of this study was to investigate the effects of low levels of zinc intake on the rat mandible and maxilla during growth and to compare these results with those of zinc-containing rats.Methods: The study was carried out on 14 Sprague-Dawley rats. The rats were randomly divided into two groups. Group I rats were fed with a Zn-deficient diet, and Group II rats with a Zn-containing diet. At the end of the fourth week on the experimental diet, all the rats were killed and blood samples were taken. Serum Zn levels were measured by atomic absorption spectrophotometry. Then, the s ulls and mandibles were freed from soft tissues and measurements were made on the dry skulls, the mandibles, and teeth in both of the two groups.Results: The zinc-deficient group showed a significantly lower value in dry skull, mandible, and teeth measurements when compared with those of the Group II.Conclusions: Changes in zinc intake might exert an effect on the growth of craniofacial structures. A low-zinc diet during adolescence might slow bone and teeth growth and enhance the risk of oral, periodontal, and orthodontic problems in later years. (Eur J Dent 2009;3:10-15)

scholarly journals Endothelial cell-derived nitric oxide mobilization is attenuated in copper-deficient rats

2008 ◽  
Vol 33 (6) ◽  
pp. 1073-1078 ◽  
Author(s):  
Jeff C. Falcone ◽  
David Lominadze ◽  
W. Thomas Johnson ◽  
Dale A. Schuschke
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelium ◽  
No Production ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Fluorescent Intensity ◽  
Consistent Finding ◽  
Cu Deficiency ◽  
Sprague Dawley Rats ◽  
Series Of Experiments

The attenuation of endothelium-dependent nitric oxide (NO) mediated vasodilation is a consistent finding in both conduit and resistance vessels during dietary copper (Cu) deficiency. Although the effect is well established, evidence for the mechanism remains circumstantial. This study was designed to determine the relative amount of NO produced in and released from the vascular endothelium. Using the fluorescent NO indicator, 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM), we now demonstrate the effect of a Cu-deficient diet on the production of NO from the endothelium of resistance arterioles. In one group of experiments, control and Cu-chelated lung microvascular endothelial cells (ECs) were used to assay NO production and fluorescence was observed by confocal microscopy. Weanling Sprague–Dawley rats were fed purified diets that were either Cu adequate (6.3 micrograms Cu per gram of food) or Cu deficient (0.3 micrograms Cu per gram of food) for 4 weeks. In the second series of experiments, first-order arterioles were microsurgically isolated from the rat cremaster muscle, cannulated, and pressurized with (3[N-morpholino]propanesulfonic acid) physiologic salt solution (MOPS-PSS). DAF-FM (5 µmol·L–1) was added in the lumen of the vessel to measure NO release. Baseline DAF-FM fluorescence was significantly lower in Cu-chelated ECs than in controls. In response to 10−6 mol·L–1 acetylcholine, fluorescent intensity was significantly less in chelated ECs and in the lumen of Cu-deficient arterioles. The results suggest that production and release of NO by the vascular endothelium is inhibited by a restriction of Cu. This inhibition may account for the attenuated vasodilation previously reported in Cu-deficient rats.

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