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PubMed1966

Biosynthesis of delta-7-cholesten-3-beta-ol, delta-5,7-cholestadien-3-beta-ol, and delta-5-cholesten-3-beta-ol by guinea pig intestinal mucosa in vitro.

Methods were developed for the separation and determination of the various 27-carbon sterols of intestinal mucosa by means of thin-layer chromatography. Scrapings of the mucosa of the small intestine of guinea pig and rat were shown to incorporate isotope from (14)C-labeled acetate and mevalonate into sterols in vitro. For each substrate this activity was lowest in mucosa from the proximal third of the small intestine and greatest in mucosa from the more distal regions of the small intestine. The total 27-carbon sterol content of guinea pig mucosa varied only slightly along the length of the small intestine, but the concentration of cholesterol was highest distally. More than 95% of the radioactivity incorporated from acetate-2-(14)C into 27-carbon sterols by guinea pig mucosa in 4 hr was recovered as lathosterol and 7-dehydrocholesterol; less than 5% was in cholesterol. The specific activities of the 27-carbon sterols were consistent with the concept that synthesis proceeds from lathosterol to 7-dehydrocholesterol to cholesterol.

Acetates↗
PubMed1991

A methylsulfonyl metabolite of a polychlorinated biphenyl can serve as a ligand for liver fatty acid binding protein in rat intestinal mucosa.

When a 100,000 x g supernatant from rat intestinal mucosa was incubated with 4,4'-bis([3H]methylsulfonyl)-2,2',5,5'-tetrachlorobiphenyl, [(CT3SO2)2TCB] a (CT3SO2)2TCB-protein complex was formed. The (CT3SO2)2TCB-protein complex was isolated and purified using gel filtration and ion-exchange chromatography. The protein portion of this complex was characterized to be liver fatty acid binding protein (L-FABP) by SDS-polyacrylamide gel electrophoresis and immunoblot analysis. No cross reactivity was observed in the immunoblot analysis between the purified protein and anti-heart or anti-intestinal fatty acid binding protein. (CT3SO2)2TCB was extractable from L-FABP and therefore not covalently bound to L-FABP.

Animals↗
PubMed1981

The effect of aspirin on mouse small-intestinal mucosa. Ultrastructural studies.

The ultrastructural alterations in the small-intestinal mucosa of mice given aspirin for five weeks were observed by light microscopy and scanning (SEM) and transmission (TEM) electron microscopy. The SEM examination revealed that the most affected areas were the duodenum and jejunum, which showed villous disarray, shortened microvilli with damaged tips, erosions, and an increased number of goblet cells. Similar findings were also observed with TEM.

Animals↗
PubMed1990

Immunologically mediated damage to the intestinal mucosa.

This review discusses experimental and clinical evidence for the existence of immunologically mediated damage to the intestinal mucosa. The discussion of mechanisms of gastrointestinal immunoregulation and lymphocyte recirculation via recently described homing receptors is preceded by a summary of the basic structures of the gut-associated lymphoid tissues (GALT). The relevance of food-induced systemic hyporesponsiveness (oral tolerance) to the prevention of immunologically mediated damage to intestinal mucosa is discussed in the light of anaphylactic (Type I) and delayed type (Type IV) hypersensitivity reactions. Other, less well defined, mechanisms of allergic injury are also briefly discussed. It is postulated that the abrogation and/or modulation of orally induced tolerance is the pathogenetic mechanism underlying the induction of food-sensitive enteropathies.

Enteritis↗
PubMed1998

Stimulation of rat hepatocyte proliferation in vitro and in vivo by factors derived from the bovine small intestinal mucosa.

A factor with a molecular weight of less than 1 kDa in the mucosa of the bovine small intestine (low molecular weight factor or LMW factor) stimulated DNA synthesis in rat hepatocytes in primary culture. This factor only showed its activity when it was added with a larger factor with a molecular weight of 30 kDa that was also found in the same tissue (high molecular weight factor or HMW factor). The LMW factor probably acts to enhance the action of a hepatotrophic growth factor, since EGF and HGF can substitute for the HMW factor. The action of the LMW factor was not due to the actions of low molecular weight substances such as norepinephrine, estradiol, triiodothyronine, and putrescine, which enhance the action of EGF or HGF, since substantial amounts of these substances were not found in the extract. When intraperitoneally administered into rats, after two-thirds hepatectomy, the LMW factor enhanced hepatocyte proliferation without the administration of the HMW factor. In the regenerating liver, a hepatotrophic growth factor(s), which acts synergistically with the LMW factor, might be properly provided, but the supply of the LMW factor might be below the level that maximally stimulates hepatocyte proliferation.

Animals↗
PubMed2006

Effect of dietary green tea catechin preparation on oxidative stress parameters in large intestinal mucosa of rats.

Intake of green tea catechin (GTC) for 4 weeks was found to elevate vitamin E level in the mucosa of the rat large intestine. Iron-induced lipid peroxidation of the mucosal homogenate was suppressed by intake of GTC in rats fed monounsaturated fatty acid (MUFA), indicating that the protective effect of dietary GTC on mucosal oxidative stress is enhanced by combination with a MUFA-rich diet.

Animals↗
PubMedDate not supplied

[Effect of estrogens on the free fatty acid content and fatty acid-binding protein fractions in rabbit intestinal mucosa].

A study was made of the effect of ovariectomy and administration of estradiol-dipropionate on the level of estrogen receptors, low molecular protein fractions, incorporating fatty acid binding proteins (FABP), and free fatty acids (FFA) in the protein fractions of the cytosol of the intestinal mucosa of mature and immature female rabbits. The female rabbit upper intestinal mucosa was shown to possess cytoplasmic estrogen receptors and to have low metabolic activity of estradiol dehydrogenase (not being target tissue). Ovariectomy caused a decrease in the level of estrogen receptors, protein fractions, incorporating FABP, and FFA in them in enterocyte mucosa cytosol as compared to respective parameters in female rabbits in the pubertal and mature periods of their development. Estrogens were involved in the regulation of the level of intestinal fatty acid binding protein fractions and in ensuring physiological concentrations of absorbed fatty acids.

Animals↗
PubMed1990

[Histochemistry of selected peptidases in small intestine mucosa in piglets experimentally infected with Isospora suis].

In the small intestine mucosa of 24 gnotobiotical piglets experimentally infected the first day post partum with oocysts of the coccidium Isospora suis, the activities of dipeptidylpeptidase IV (EC.3.4.14.5.; DAP IV) and gamma-glutamyl transferase (EC.2.3.2.2.; GGT) in the microvillous zone of enterocytes were evaluated by scanning densitometry. The tissue of the small intestine in piglets infected with a dose of 100,000 oocysts of the coccidia of I. suis was examined in the period from the first till the eleventh day post infection (DPI). In the control piglets at the age of 2-5 days it was found that most of the DAP IV activity was located in the microvillous zone of the enterocytes of the middle jejunum, rear jejunum and ileum. The DAP IV activity of duodenum mucosa was lower; as compared with the activity in the mucosa of the jejunum and ileum it reached 53-57%. In the case of GGT activity, the highest density values of the reaction product were recorded in the microvillous zone of enterocytes of the duodenum and the whole jejunum, the lowest in the ileum mucosa (86-89%) of the activity found in the duodenum and jejunum). During the experimental infection the infected piglets had a significant deficit of both peptidases, especially DAP IV (the whole studied period). The development of GGT activity was slightly different with the onset of the marked decline of the enzyme activity only on the fifth DPI. The lower GGT activity persisted till the eighth DPI. The density of the GGT reaction product began to return to the normal on the ninth to eleventh DPI. No predisposition in the location of the deficit was observed in the peptidases studied during the infection. The decline of the activity of both enzymes influenced also the mucosa of all studied parts of the small intenstine. The difference lay in the relevance of lowering of the density of reaction product of DAP IV and GGT on other DPI and in the different intensities of the return of the activity to the physiological normal.

Animals↗
PubMed1980

Effect of fasting on Na-K-ATPase activity in rat small intestinal mucosa.

The effect of fasting on mucosal Na-K-ATPase activity in various regions of rat small intestine was investigated. Fasting (17--48 h) was associated with a consistent decrease in specific and total activity of Na-K-ATPase in the jejunum, the levels tending to rise more distally. No effect on the specific activities of Mg-ATPase or alkaline phosphatase was found. Fasting was also associated with incresed adrenocortical activity and with decreases in mucosal mass, protein content, and histological dimensions of the jejunum, no similar changes being found in the distal small intestine. Glucose ingestion prevented the decrease in jejunal enzyme activity associated with fasting and elevated levels in the mid and terminal small intestine of fed animals. These effects suggest that Na-K-ATPase activity in small intestinal mucosa may be, in part, inducible.

Alkaline Phosphatase↗
PubMed1983

Purification and properties of an acid deoxyribonuclease from rat small intestinal mucosa.

An acid deoxyribonuclease has been purified from rat small intestinal mucosa by a procedure including ammonium sulfate fractionation, chromatographies on DEAE-cellulose, CM-cellulose and SE-Sephadex and finally isoelectric focusing. Polyacrylamide gel electrophoresis of the purified enzyme preparation showed one major and two minor bands, and the enzyme activity corresponded to one of the minor bands. The enzyme preparation was free of contaminating DNase I, DNase III, alkaline RNase, acid and alkaline phosphatases and nonspecific phosphodiesterase, but slight activities of DNase IV and acid RNase were detected. The enzyme did not require divalent cations for activity, had a pH optimum of 4.5 in 0.33 M sodium acetate buffer, and had an optimum temperature of 50 to 60 degrees C when assayed for 30 min. The rate of hydrolysis of native DNA was about 2.5-fold faster than that observed with denatured DNA. Its molecular weight was found to be 9.0 +/- 0.1. The enzyme catalyzes the endonucleolytic cleavage of native and denatured DNA, yielding oligonucleotides which have an average chain length of about 7, and which contain 3'-phosphoryl termini. The mode of action of the enzyme is double-strand scission.

Animals↗
PubMed1987

Adhesion of enteropathogenic Escherichia coli to human intestinal enterocytes and cultured human intestinal mucosa.

The adhesion of classic enteropathogenic Escherichia coli (EPEC) strains of human origin to isolated human small intestinal enterocytes and cultured small intestinal mucosa was investigated. An adhesion assay with isolated human enterocytes prepared from duodenal biopsy samples was developed and tested with EPEC strains known to cause diarrhea in healthy adult volunteers. In the assay a mean of 53 and 55% of enterocytes had brush border-adherent E. coli E2348 (O127;H6) and E851 (O142:H6), respectively, whereas the value for a nonpathogenic control strain and a plasmid-cured derivative of strain E2348 was 0%. A collection of 17 EPEC strains was also tested for the ability to colonize cultured human duodenal mucosa. Extensive colonization occurred with 13 strains, including serogroups O55, O86, O111, O114, O119, O127, O128, and O142; and in each case electron microscopic examination of colonized mucosa revealed the characteristic histopathological lesion reported by others in natural and experimental EPEC infections. EPEC strains were seen to adhere intimately to the enterocyte surface, causing localized destruction of microvilli. The plasmid-cured derivative of strain E2348, which colonized cultured mucosa much less efficiently than the parent strain, nevertheless produced an identical lesion, indicating that plasmid-encoded factors are not essential for adhesion and the brush border-damaging property of EPEC.

Bacterial Adhesion↗
PubMed1999

Influence of physicochemical and biological parameters on drug release from microspheres adhered on vesical and intestinal mucosa.

The object of our work is to develop mucoadhesive microspheres to be applied into the urinary bladder. In the present study the microspheres were prepared and the release of a model drug after their adhesion to mucosa was evaluated. The microspheres were prepared by solvent evaporation method using Eudragit RL or hydroxypropylcellulose as matrix polymers and one out of five different polymers as mucoadhesives or non-mucoadhesive references. A method for the evaluation of the drug release from microspheres adhered on guinea pig urinary bladder and small intestine mucosa was developed and the influence of the following parameters on this process was followed: mucoadhesion strength of polymeric films, swelling of polymers and the drug release from microspheres. The results showed that the detachment forces were decreasing in the following order: CMCNa > Carbopol 934P > HPC > EE.HCl = PVP/VA. Carbopol swelled to the largest volume among all polymers and the drug release from microspheres was more retarded when Eudragit RL was used as matrix polymer. When comparing the results of pipemidic acid release from microspheres adhered on intestinal mucosa with detachment forces, similar ratios among the mucoadhesive polymers can be seen. On the other hand, differences between two mucosae were observed. These differences are due to the amount of mucus on mucosa and might also be influenced by the charge of mucus. The goal of our work at this point of investigation was achieved by microspheres containing carboxymethylcellulose as mucoadhesive and Eudragit RL as matrix polymer because they provide the longest release time from microspheres adhered on vesical mucosa and sufficient high strength of mucoadhesion.

Acrylic Resins↗
PubMed1999

Identification of an adhesion molecule expressed on adult T cell leukemia cells derived from a patient with gastrointestinal involvement: implication for a possible role of integrin beta 7 in leukemic cell infiltration into intestinal mucosa.

Patients with adult T cell leukemia (ATL) often manifest leukemic cell infiltration into various organs such as lung, liver, skin, and gut. To analyze the mechanism of intestinal infiltration of ATL cells, we made mAbs against ATL-43T, a human T cell line derived from an ATL patient with severe intestinal mucosal infiltration. One of the mAbs, named H920, was noted for a high and relatively specific reactivity with ATL-43T. Molecular cloning was done to identify this molecule and disclosed that the Ag molecule was identical to integrin beta 7. Since integrin beta 7 and its ligand MAdCAM-1 had been reported to mediate homing of lymphocytes to endothelial cells in intestinal mucosa, we next examined wither ATL-43T cells could adhere to MAdCAM-1+ cells. Human MAdCAM-1 transfectants of MMCE, a mouse epithelial cell line, were made and used to evaluate cell adhesion mediated by integrin beta 7 and MAdCAM-1. Considerable levels of cell adhesion were observed between ATL-43T and the transfectant cells, which was inhibited by H920 mAb in a dose-dependent manner. Furthermore, peripheral blood leukemic cells or lymphoma cells from 10 ATL patients were examined for expression of integrin beta 7 with regard to organ involvement. Samples from three patients with gastrointestinal tract involvement showed considerably higher expression of integrin beta 7. These results suggest that integrin beta 7 may play a role in adhesion and subsequent infiltration of a certain type of ATL cells into intestinal mucosa.

Adult↗
PubMed2006

Gene expression in human small intestinal mucosa in vivo is mediated by iron-induced oxidative stress.

Iron-induced oxidative stress in the small intestine may alter gene expression in the intestinal mucosa. The present study aimed to determine which genes are mediated by an iron-induced oxidative challenge in the human small intestine. Eight healthy volunteers [22 yr(SD2)] were tested on two separate occasions in a randomized crossover design. After duodenal tissue sampling by gastroduodenoscopy, a perfusion catheter was inserted orogastrically to perfuse a 40-cm segment of the proximal small intestine with saline and, subsequently, with either 80 or 400 mg of iron as ferrous gluconate. After the intestinal perfusion, a second duodenal tissue sample was obtained. Thiobarbituric acid-reactive substances, an indicator of lipid peroxidation, in intestinal fluid samples increased significantly and dose dependently at 30 min after the start of perfusion with 80 or 400 mg of iron, respectively (P < 0.001). During the perfusion with 400 mg of iron, the increase in thiobarbituric acid-reactive substances was accompanied by a significant, momentary rise in trolox equivalent antioxidant capacity, an indicator of total antioxidant capacity (P < 0.05). The expression of 89 gene reporters was significantly altered by both iron interventions. Functional mapping showed that both iron dosages mediated six distinct processes. Three of those processes involved G-protein receptor coupled pathways. The other processes were associated with cell cycle, complement activation, and calcium channels. Iron administration in the small intestine induced dose-dependent lipid peroxidation and a momentary antioxidant response in the lumen, mediated the expression of at least 89 individual gene reporters, and affected at least six biological processes.

Adult↗
PubMed1994

Cell kinetics and polyamine enzymes in the intestinal mucosa of rats with azoxymethane induced tumours.

We studied the proliferative activity and the modifications in ornithine decarboxylase (ODC) and diamine oxidase (DAO), enzymes involved in polyamine metabolism, in the apparently normal intestinal mucosae of rats with azoxymethane induced tumours. Fifty rats were treated with six weekly injections of 15 mg/kg body weight azoxymethane (AOM). Six rats died during the treatment. All the surviving rats developed intestinal tumours; tumour incidence was 93.1% (41/44) in the left colon, 40.9% (18/44) in the right colon and 45.4% (20/44) in the small bowel. In the normal-appearing mucosa close to intestinal tumours we found an extension of the normal proliferative compartment to the upper third of the crypts (stage I abnormality) and a shift of most of the DNA synthesizing cells from the basal region to the middle and upper third (stage II abnormality). Furthermore, the intestinal mucosa characterized by proliferative abnormalities showed an ODC activity significantly higher than the normal mucosa of control rats (small bowel: 1.01 +/- 0.26 vs 0.42 +/- 0.15, P < 0.01; right colon: 1.32 +/- 0.34 vs 0.25 +/- 0.02, P < 0.001; left colon: 1.93 +/- 0.35 vs 0.22 +/- 0.01, P < 0.01). We also detected a significant decrease of DAO activity in the mucosa of the small bowel and right colon of treated rats compared to controls (0.86 +/- 0.09 vs 4.39 +/- 0.85, P < 0.01; 1.04 +/- 0.43 vs 3.80 +/- 0.91, P < 0.01, respectively), while DAO activity in the left colon was unchanged. The lower incidence of tumours in the small bowel and right colon suggests the presence of factors protecting these segments from carcinogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Amine Oxidase (Copper-Containing)↗
PubMed1976

Ribosome structure and chylomicron formation in rat intestinal mucosa.

Sucrose gradient sedimentation and electron micrographic studies were made on the ribosomes of the cells of intestinal mucosa isolated from control, bile fistula, and puromycin-treated rats. In comparison to controls, there was a 40 to 60 per cent decrease in polysome content of the cells following administration of puromycin or deprivation of luminal choline by creation of a bile fistula. Feeding of lysolecithin of choline to the bile fistula rats or addition to the isolated cells in vitro resulted in a complete restoration of the polysome profile along with lipprotein synthesis and chylomicron release. Addition of lysolecithin to isolated cells treated with puromycin in vitro also brought about a reaggregation of the ribosomes and a reactivation of phospholipid biosynthesis. Choline had no detectable effect on phospholipid synthesis or ribsosme aggregation when fed to ppuromycin-treated rats or when added to puromycin-treated cells in vitro. The results suggest that chylomicron formation and the release by the muscosal cells depend upon intact rough endoplasmic reticulum and an active protein adn phospholipid biosynthesis. The role of lysolecithin in this process is ratonalized on the basis of its ability to supply a precursor of lecithin as well as a surfactant which affects the aggregation, or membrane rebinding of ribosomes, or both.

Animals↗
PubMed1978

Regulation of cholesterol synthesis in cultured canine intestinal mucosa.

The regulation of intestinal cholesterol synthesis was studied utilizing canine ileal mucosa maintained in organ culture for 6 h. Viability was monitored by light and electron microscopy, measurement of cellular enzymes, and the ability to actively transport a glucose analogue. The activity of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (EC 1.1.4.3.4), the rate-limiting enzyme of cholesterol synthesis, increased 4-fold during a 6-h culture. A parallel increase occurred in the rate of acetate incorporation into digitonin-precipitable sterols during this period. This increase could be prevented by the addition of cycloheximide to the culture. Pure cholesterol, 7-ketocholesterol, and 25-hydroxycholesterol, when present during the last 4 h of culture, also caused significant suppression of the rise in HMG-CoA reductase activity (final HMG-CoA reductase with the three sterols was 77 +/- 4%, 68 +/- 5%, and 58 +/- 3% of control postculture value). Bile salts at low, nontoxic concentrations also inhibited the increase of enzyme activity (2 mM taurocholate = 63 +/- 3% of control, 0.5 mM taurochenodeoxycholate = 76 +/- 6% of control). In contrast, dog lipoproteins separated by ultracentrifugation failed to significantly affect intestinal cholesterol synthesis in these short term organ cultures.

Animals↗