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At least 163 records · Page 9Linked to original sources
PubMed1993

Metabolism of sulfonate analogs of ursodeoxycholic acid and their effects on biliary bile acid composition in hamsters.

The metabolism of sodium 3 alpha,7 beta-dihydroxy-5 beta-cholane-24-sulfonate and sodium 3 alpha,7 beta-dihydroxy-24-nor-5 beta-cholane-23-sulfonate was studied in hamsters. In bile fistula animals these sulfonate analogs of ursodeoxycholic acid were absorbed mainly from the terminal ileum and secreted rapidly into the bile without biotransformation or conjugation. After oral administration, the sulfonate analogs were excreted in the feces at the same rate as chenodeoxycholic acid and its metabolic products. The intestinal microorganisms transformed chenodeoxycholic acid largely into lithocholic acid; the sulfonate analogs were completely resistant to biotransformation. After a 2-week feeding period, the sulfonate analogs of ursodeoxycholic acid accounted for 24.0% and 16.9% of total biliary bile acids. These sulfonates did not affect the proportions of the natural bile acids in the bile, and the ratio of glycine-conjugated bile acids to taurine-conjugated bile acids was not altered by feeding the sulfonates. In contrast, when ursodeoxycholic acid was fed, the proportions of the natural bile acids and the glycine/taurine ratio were changed. These results suggest that the sulfonate analogs had no profound effect on endogenous bile acid metabolism and did not cause a depletion of the hepatic taurine pool during enterohepatic circulation. The sulfonates had no effect on intestinal cholesterol absorption and serum cholesterol levels.

Animals↗
PubMed2006

Fatal enterocolitis in Asian elephants (Elephas maximus) caused by Clostridium difficile.

Two cases of fatal enteritis caused by Clostridium difficile in captive Asian elephants are reported from an outbreak affecting five females in the same zoo. Post mortem examination including histopathology demonstrated fibrinonecrotic enterocolitis. C. difficile was isolated by selective cultivation from two dead and a third severely affected elephant. Four isolates were obtained and found positive for toxin A and B by PCR. All isolates were positive in a toxigenic culture assay and toxin was demonstrated in the intestinal content from one of the fatal cases and in a surviving but severely affected elephant. PCR ribotyping demonstrated that the C. difficile isolates shared an identical profile, which was different from an epidemiologically unrelated strain, indicating that the outbreak was caused by the same C. difficile clone. It is speculated that the feeding of large quantities of broccoli, a rich source of sulforaphane, which has been shown to inhibit the growth of many intestinal microorganisms may have triggered a subsequent overgrowth by C. difficile. This is the first report of C. difficile as the main cause of fatal enterocolitis in elephants. The findings emphasize the need to regard this organism as potentially dangerous for elephants and caution is recommended concerning antibiotic treatment and feeding with diets containing antimicrobials, which may trigger an expansion of a C. difficile population in the gut.

Animals↗
PubMed2003

Mpi recombinase globally modulates the surface architecture of a human commensal bacterium.

The mammalian gut represents a complex and diverse ecosystem, consisting of unique interactions between the host and microbial residents. Bacterial surfaces serve as an interface that promotes and responds to this dynamic exchange, a process essential to the biology of both symbionts. The human intestinal microorganism, Bacteroides fragilis, is able to extensively modulate its surface. Analysis of the B. fragilis genomic sequence, together with genetic conservation analyses, cross-species cloning experiments, and mutational studies, revealed that this organism utilizes an endogenous DNA inversion factor to globally modulate the expression of its surface structures. This DNA invertase is necessary for the inversion of at least 13 regions located throughout the genome, including the promoter regions for seven of the capsular polysaccharide biosynthesis loci, an accessory polysaccharide biosynthesis locus, and five other regions containing consensus promoter sequences. Bacterial DNA invertases of the serine site-specific recombinase family are typically encoded by imported elements such as phage and plasmids, and act locally on a single region of the imported element. In contrast, the conservation and unique global regulatory nature of the process in B. fragilis suggest an evolutionarily ancient mechanism for surface adaptation to the changing intestinal milieu during commensalism.

Bacterial Capsules↗
PubMed1980

Ligandin: an adventure in liverland.

Ligandin is an abundant soluble protein which has a t 1/2 of 2--3 days, is induced by many drugs and chemicals, and is stabilized in the absence of thyroid hormone. The protein is strategically concentrated in cells associated with transport and detoxification of many endogenous ligands, such as bilirubin, and exogenous ligands, such as drugs and chemicals. The protein is a dimer in rat liver. Whether the dimer is a primary gene product or at least two genes are involved is not known. The protein has broad, low affinity catalytic activity as a GSH-S-transferase for many ligands having electrophilic groups and hydrophobic domains. It catalyzes formation of GSH conjugates, non-covalently binds some ligands prior to their biotransformation or excretion in bile, and covalently binds other ligands, such as activated carcinogens. Recent studies include the possible role of ligandin in chemical carcinogenesis, diagnosis of inflammatory and neoplastic disease of the liver and kidney, and participation in intracellular transport. Although some of the roles that have been outlined are speculative, any single function is important. The GSH-S-transferases are primitive enzymes and non-specific binding proteins but "it is precisely their simplistic design that allows such protean serviceability". Ligandin illustrates a group of hepatic disposal mechanisms which involve bulk transport of ligands. Although specific uptake and transport mechanisms have been described for several hormones which enter the hepatocyte in small quantities and regulate intermediary metabolism and, possibly, cell maturation, bulk transport of ligands into, through and out of the liver involves mechanisms which accomodate many metabolites, drugs and chemicals of diverse structure. The liver is bathed in sewage which contains what we ingest or are injected with and potentially toxic products of intestinal microorganisms. The chemical formulas of the many substances which are metabolized by the liver provide a horror show of potentially reactive and toxic metabolites, mutagens and carcinogens. Despite this alimentary "Love Canal", we and our livers do remarkably well. These hepatic disposal mechanisms, as exemplified by ligandin, evolved in ancient times. They are present, albeit sluggishly, in insects and ancient elasmobranchs. Hepatic uptake and removal mechanisms of high capacity, modest affinity and broad substrate range permit us to live in what has probably always been a threatening world.

Animals↗
PubMed1999

Metabolism and excretion of ochratoxin A fed to sheep.

Hydrolysis of the mycotoxin ochratoxin A (OA) to ochratoxin alpha (Oalpha) by microorganisms within the gastrointestinal tract leads to the excretion of OA as the nontoxic alpha form. The Oalpha form is the principal means for the detoxification of OA. In the current experiment, three groups of four sheep were fed diets consisting of 70% concentrates and 30% hay (dry matter basis, energy to supply 1.1 times the requirement for maintenance) for 4 wk with three dietary concentrations of OA (0, 2, or 5 mg/kg of concentrate feed). The OA content did not affect feed intake or nutrient digestibility. In a preliminary experiment, an OA dose of 20 mg/kg of concentrate feed greatly reduced feed intake. After 1, 2, 3, and 4 wk of the trial, significant concentrations of OA were detected in the serum of the animals fed 2 or 5 mg of OA/kg feed. This suggested that even at a dosage of 2 mg of OA/kg of concentrate feed, considerable amounts of OA were not degraded by ruminal and intestinal microorganisms. The analysis of the feces and urine samples reflected these findings; OA and Oalpha were found in significant concentrations, escaping fermentation in the rumen and in the hindgut. The current experiment demonstrates that OA hydrolysis in the gastrointestinal tract of sheep is substantially less than previously described, especially if OA is ingested in combination with concentrate-rich diets.

Administration, Oral↗
PubMed1977

Immune responses to environmental antigens absorbed through the gastrointestinal tract.

Foods, food additives, beverages, drugs, and intestinal microorganisms are potentially important sources of environmental antigens. While proteins taken orally ordinarily are absorbed to only a limited extent, under appropriate circumstances enough absorption occurs to produce an immune response. Acute allergic reactions to foods are not uncommon and as a rule are mediated by IgE antibodies. The possibility that small quantities of food antigens absorbed over a period of years without acute symptoms of allergy might produce a cumulative systemic or local immunological toxicity remains to be convincingly demonstrated.

Age Factors↗
PubMed1985

Biosynthesis of cholestanol from bile acid intermediates in the rabbit and the rat.

Biliary 7 alpha-hydroxy-4-cholesten-3-one (an intermediate in bile acid biosynthesis) may be 7 alpha-dehydroxylated in the gut and further metabolized to cholestanol (Skrede, S., and Björkhem, I. (1982) J. Biol. Chem. 257, 8363-8367). We have now evaluated the quantitative importance of pathway(s) to cholestanol with 7 alpha-hydroxylated C27 steroids as intermediates. After feeding conventionally fed rabbits or rats or germ-free rats with [7 alpha-3H]cholesterol and [4-14C]cholesterol, tissue cholestanol could be isolated with about a 20% lower 3H/14C ratio than present in cholesterol. We conclude that there is a pathway to cholestanol involving 7 alpha-hydroxylated intermediates. Intestinal microorganisms are not essential for this pathway, which accounts for at most 20% of the cholestanol formed in these species. In bile fistula rats, there was also a significant conversion of intraperitoneally injected [7 beta-3H]7 alpha-hydroxycholesterol and [4-14C]7 alpha-hydroxy-4-cholesten-3-one into cholestanol. The enzymes involved in the 7 alpha-hydroxylation/dehydroxylation pathway for the biosynthesis of cholestanol are probably located in the liver. Both 7 alpha-hydroxycholesterol and 7 alpha-hydroxy-4-cholesten-3-one may be intermediates.

Animals↗
PubMed1994

[Microbial translocation from the gastrointestinal tract--pathophysiologic phenomenon or catalyst for multiple organ failure?].

The constant passage of intestinal microorganisms and endotoxin into the gut associated immune system is an important physiological process for its optimal function. Under the conditions of disturbed microflora homeostasis, impaired mucosal permeability, and immunocompromisation, translocation is pathologically increased both in the animal experiment and in man. The clinical relevance of increased translocation is not yet definitively established. But from lots of evidence it seems that in the immunocompromised critically ill with systemic inflammatory response syndrome/sepsis, microbial translocation plays an important role for the eventual outcome towards multiple-organ-failure. Our therapeutic efforts have to concentrate on protection of the gut mucosa by maintaining adequate splanchnic blood flow and providing early enteral nutrition.

Acute-Phase Reaction↗
PubMed1990

Antibiotic-induced vitamin K deficiency and the role of the presence of intestinal flora.

Cephalosporin antibiotics with N-methyl-thio-tetrazole (NMTT) side chains have been known to be associated with the development of hypoprothrombinemia. However, it has not been fully established whether these symptoms are induced by an inhibition of vitamin K production by intestinal microorganisms or by an inhibitory action of these antibiotics on endogenous vitamin K metabolism. Therefore, an attempt has been made to clarify the above-mentioned ambiguity by using germfree mice in which primary vitamin K deficiency can be established within a short experimental period. Germfree (GF) and conventional (CV) ICR male mice, 8-13 weeks old were used in this experiment. Vitamin K deficient (Def) and menaquinone-4 supplemented diet (MK-4) were fed to the mice in both rearing conditions. In the antibiotic-treated group, sodium latamoxef (LMOX, 300 mg/kg B.W./day) was intraperitoneally administered once a day, and in the control group the same volume of saline (Saline) was administered. Severe vitamin K deficient symptoms were observed in the GF-K-Def-LMOX group, and both prothrombin time (PT) and activated-partial thromboplastin time (APTT) values were prolonged on the 8th day of the experimental period compared with the GF-K-Def-Saline group. Furthermore the mortality rate of GF-K-Def-LMOX group was comparatively higher than that of the Saline group. This study has provided evidence that vitamin K deficiency is amplified by an administration of LMOX even in the absence of intestinal flora.

Animals↗
PubMed1998

Toxicological aspects on the release and systemic uptake of mercury from dental amalgam.

This paper summarizes some recent reports on mercury release from amalgam fillings and resulting concentrations in biological fluids, development of antibiotic resistance, and kidney function. In a series of studies of subjects with amalgam fillings, mercury (Hg) levels were followed in saliva, feces, blood, plasma, and urine before and until 60 d after removal of all of the fillings. The Hg concentrations in saliva remained elevated for at least 1 wk, suggesting that dissolved Hg vapor is not the major source of mercury in mixed saliva. An absorption phase of Hg was seen in plasma during 24 h after amalgam removal. After 60 d the plasma Hg concentration was reduced to 40%, of the baseline level. The decrease per amalgam surface was 0.11 nmol/l (range 0.02 0.40). The Hg level in feces increased two orders of magnitude two days after amalgam removal. At day 60, the median Hg concentration was still slightly higher than the median value of the amalgam free control group. The resistance patterns of the oral and intestinal microflora in these subjects were also studied. In the intestinal microflora, the relative amount of intestinal microorganisms resistant to 50 microM HgCl2 peaked 7 d after removal of the amalgam fillings, with a median value per sample of 6.1%, compared to 1.3% in samples collected prior to the Hg exposure. However, no statistical differences in the resistance pattern of the oral microflora were detected between the control and the experimental groups. A number of sensitive kidney function parameters were measured 1 wk before and 1, 2, and 60 d after amalgam removal. No effects on the various kidney parameters studied were recorded. According to the conclusions of independent evaluations from different state health agencies, the release of mercury from dental amalgam does not present any non-acceptable risk to the general population.

Absorption↗
PubMed2000

Ecological disturbances in intestinal microflora caused by clinafloxacin, an extended-spectrum quinolone.

BACKGROUND: The quinolones developed over the past few years have enhanced in vitro activity and a broader spectrum of antimicrobial activity compared to many other antimicrobial agents including the older quinolones. The present study focuses on the effect of clinafloxacin, a member of the new broad-spectrum quinolone class of antibiotics, on the normal intestinal microflora. SUBJECTS AND METHODS: A total of 12 healthy volunteers received clinafloxacin orally, 200 mg twice daily for 7 days. Fecal specimens were collected at defined intervals before, during and after the administration in order to study the effect of clinafloxacin on the intestinal microflora and to correlate this effect with fecal clinafloxacin concentrations. Intestinal microorganisms isolated before, during and 2 weeks after clinafloxacin administration were tested for their suseptibility to clinafloxacin. RESULTS: Oral administration of clinafloxacin resulted in high drug levels in feces (mean value 176.2 mg/kg on day 7) and pronounced ecological disturbances. The aerobic microflora was eradicated in 11 of the 12 subjects and the anaerobic microflora was strongly suppressed during administration. There was a significant emergence of clinafloxacin-resistant Bacteroides spp. strains (MIC > or = 4 mg/ml) during administration. The elevated MIC values still remained 2 weeks after discontinuation of the antibiotic (p < 0.001). CONCLUSION: The emergence of clinafloxacin-resistant Bacteroides spp. demonstrates the necessity of restricting prescription for particular indications in order to preserve the efficacy of the highly active broad-spectrum quinolones.

Administration, Oral↗
PubMed1998

Safflower oil consumption does not increase plasma conjugated linoleic acid concentrations in humans.

Conjugated linoleic acid (CLA) is a mixture of positional and geometric isomers of linoleic acid (LA) with conjugated double bonds. CLA has anticarcinogenic properties and has been identified in human tissues, dairy products, meats, and certain vegetable oils. A variety of animal products are good sources of CLA, but plant oils contain much less. However, plant oils are a rich source of LA, which may be isomerized to CLA by intestinal microorganisms in humans. To investigate the effect of triacylglycerol-esterified LA consumption on plasma concentrations of esterified CLA in total lipids, a dietary intervention (6 wk) was conducted with six men and six women. During the intervention period a salad dressing containing 21 g safflower oil providing 16 g LA/d was added to the subjects' daily diets. Three-day diet records and fasting blood were obtained initially and during dietary and postdietary intervention periods. Although LA intake increased significantly during the dietary intervention, plasma CLA concentrations were not affected. Plasma total cholesterol and LDL-cholesterol concentrations were significantly lower after addition of safflower oil to the diet. In summary, consumption of triacylglycerol-esterified LA in safflower oil did not increase plasma concentrations of esterified CLA in total lipids.

Adult↗
PubMed2005

Nocturnal production of endospores in natural populations of epulopiscium-like surgeonfish symbionts.

Prior studies have described a morphologically diverse group of intestinal microorganisms associated with surgeonfish. Despite their diversity of form, 16S rRNA gene surveys and fluorescent in situ hybridizations indicate that these bacteria are low-G+C gram-positive bacteria related to Epulopiscium spp. Many of these bacteria exhibit an unusual mode of reproduction, developing multiple offspring intracellularly. Previous reports have suggested that some Epulopiscium-like symbionts produce dormant or phase-bright intracellular offspring. Close relatives of Epulopiscium, such as Metabacterium polyspora and Clostridium lentocellum, are endospore-forming bacteria, which raises the possibility that the phase-bright offspring are endospores. Structural evidence and the presence of dipicolinic acid demonstrate that phase-bright offspring of Epulopiscium-like bacteria are true endospores. In addition, endospores are formed as part of the normal daily life cycle of these bacteria. In the populations studied, mature endospores were seen only at night and the majority of cells in a given population produced one or two endospores per mother cell. Phylogenetic analyses confirmed the close relationship between the endospore-forming surgeonfish symbionts characterized here and previously described Epulopiscium spp. The broad distribution of endospore formation among the Epulopiscium phylogenetic group raises the possibility that sporulation is a characteristic of the group. We speculate that spore formation in Epulopiscium-like symbionts may be important for dispersal and may also enhance survival in the changing conditions of the fish intestinal tract.

Animals↗
PubMed2005

Five years of research on health risks and benefits of Maillard reaction products: an update.

When the COST Action 919 started to investigate the role of melanoidins in food and health in 1999, the chemical structures of dietary melanoidins were poorly defined and hardly anything was known about structure-specific health effects of this chemical class. In addition, the degradation of melanoidins in the gut and their absorption and function or that of any of their degradation products had not yet been reported. In the past five years, results from in vitro studies demonstrated that at least some of the dietary melanoidins are degraded by intestinal microorganisms, possibly influencing their growth rate. The absorption and excretion rates of individual Maillard reaction compounds and melanoidin structures have been investigated in animal studies. These studies show that at least 30% of the ingested dose of low-molecular-weight compounds are absorbed. Structure-specific health-promoting effects of newly identified compounds have been described by means of their antioxidant and chemopreventive activity in cell culture investigations as well as in animal feeding studies and human trials. Harmful effects of dietary melanoidins have been investigated in the context of their ability to promote glycation reactions in vivo, which are involved in the progression of several diseases, such as diabetes mellitus, cardiovascular complications, and Alzheimer's disease. Toxicological studies were performed showing that melanoidin structures can not be classified as potent dietary mutagens or genotoxins. Thus, substantial knowledge on the health effects of melanoidins has been gained within COST Action 919. But still, further studies are needed to distinguish between chemically identified harmful and health-beneficial melanoidins.

Antioxidants↗
PubMed2004

Differential effect of ginsenoside metabolites on the 5-HT3A receptor-mediated ion current in Xenopus oocytes.

Ginsenosides are major active ingredients of Panax ginseng. They have a number of pharmacological and physiological actions and are transformed into compound K (CK) or M4 by intestinal microorganisms. CK is derived from protopanaxadiol (PD) ginsenosides, whereas M4 is derived from protopanaxatriol (PT) ginsenosides. Recent reports show that ginsenosides act as pro-drugs for these metabolites. In previous work we demonstrated that the ginsenoside Rg2 regulates human 5-hydroxytryptamine3A (5-HT3A) receptor channel activity [Choi et al. (2003)]. In the present study, we investigated the effect of CK and M4 on the activity of the human 5-HT3A receptor channel. The 5-HT3A receptor was expressed in Xenopus oocytes, and the current was measured using the two-electrode voltage clamp technique. Treatment with CK or M4 had no effect on oocytes injected with 5-HT3A receptor cRNA. However pretreatment with M4 or CK followed by injection of 5-HT3A receptor cRNA led to reversible inhibition of the 5-HT-induced inward peak current (I(5-HT)). Half maximal inhibitory concentrations (IC50) of CK and M4 were 36.9 +/- 9.6 and 7.3 +/- 2.2 microM, respectively. Inhibition by M4 was non-competitive and voltage-independent. These results indicate that M4, a metabolite of PT ginsenosides, acts primarily on 5-HT3A receptors and further, that ginsenosides as well as ginsenoside metabolites can influence 5-HT3A receptor channel activity in Xenopus oocytes.

Animals↗
PubMed1997

Preferential binding with Escherichia coli hsp60 of antibodies prevalent in sera from patients with rheumatoid arthritis.

One hundred thirty-two patients with various connective tissue disorders, including 60 with rheumatoid arthritis (RA), had antibodies against human as well as Escherichia coli hsp60 in titers significantly higher than those of normal controls. There was a correlation between titers of antibody to human hsp60 and those to E. coli hsp60. Levels of antibodies against human and E. coli hsp60 were lower in joint fluids than in sera, indicating little production of antibodies in the joint. Antibodies affinity-purified with E. coli hsp60 bound strongly with the homologous hsp60, but weakly with human hsp60. However, antibodies affinity-purified with human hsp60 bound comparably with both E. coli hsp60 and human hsp60. Antibodies affinity-purified with Mycobacterium tuberculosis hsp65 bound to human hsp60 with a reactivity similar to the reactivity of those affinity-purified with human hsp60. The reactivity to the three hsp60 species was lost when sera were absorbed with E. coli hsp60, while the reactivity to E. coli hsp60 remained after extensive absorption with M. tuberculosis hsp65 or human hsp60. These results indicate that anti-hsp60 antibodies in patients with RA and other connective tissue disorders are raised by infection with intestinal microorganisms such as E. coli. They may represent another example of autoimmune responses triggered by antigenic mimicry of host proteins to microbes and suggest that the reactivity of antibodies from RA patients with M. tuberculosis hsp65 might have been a cross-reaction with the E. coli homologue.

Antibodies↗