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At least 181 records · Page 10Linked to original sources
PubMed1978

Development of the IgA system in the mammary gland.

1) Lymphoblasts in gut-associated lymphoid tissue, committed to the production of IgA, can home to the mammary glands of syngeneic mice and differentiate there into IgA-containing plasmablasts. The phenomenon is limited to near term and lactating recipients. 2) The ability of lymphocytes originating in gut-associated lymphoid tissue and sensitized to intestinal antigens to migrate to the mammary gland can account for the specificity of milk IgA toward intestinal microorganisms and the consequent passive protection offered to suckling infants. 3) The secretory immune system of the mammary gland is apparently under hormonal control since mammotropic hormones given to virgin females can induce morphological and functional characteristics seen naturally only during pregnancy and lactation. Examples are increased numbers of IgA plasma cells and the ability to trap their circulating precursors taken from mesenteric lymph nodes.

Animals↗
PubMed1982

Antibacterial and antimycotic effect of a newly discovered secretion from larvae of an endoparasitic insect, Pimpla turionellae L. (hym.).

The larvae of Pimpla turionellae, that develop in pupae of various Lepidoptera, discharged through their anus up to 8 microliters/h of a hyaline liquid, which is termed "anal secretion". It exerted a strong bacteriostatic effect on Enterobacter cloacae, a highly virulent intestinal microorganism isolated from the midgut of the host pupa, Pieris brassicae. Growth inhibition of Escherichia coli, Micrococcus luteus and Pseudomonas phaseolicola was also evident, but less pronounced. Inhibition depended upon the concentration of the anal secretion. This was also true regarding the effect on growth of Beauveria bassiana, a fungus pathogenic on insects. The antimycotic action of the anal secretion was less effective against Chaetomium pululiferum, a soil-inhabiting fungus. Growing hyphae of B. bassiana were malformed, exhibiting the so-called "curling effect", when treated with anal secretion. Parenteral injection of a low dose of Enterobacter cloacae resulted in 100% mortality of non parasitized pupae of Pieris brassicae; however, simultaneous injection of 3 microliters of anal secretion resulted in higher survival.

Anal Canal↗
PubMed1981

Recontamination after gastrointestinal decontamination with non-absorbable antibiotics.

In an attempt to restore the colonization resistance we administered anaerobic microflora to prevent an abnormal colonization of the intestine after antibiotic treatment had been discontinued. After the antibiotics had been discontinued and before the donor flora had been administered and had colonized the intestine, microorganisms present were "unopposed" and expanded to a high density. A mouse model was used to investigate which antibiotics negatively influenced the donor flora and reduced the colonization resistance when administered intraperitoneally. Erythromycin, clindamycin and carbenicillin suppressed the donor flora permanently, as could be seen by the reduced colonization resistance. Benzylpenicillin, ampicillin, doxycycline and the combination gentamicin-cephalothin affected the colonization resistance as long as these agents were present. Gentamicin alone and cephalothin and oxytetracycline had no effect on the colonization resistance.

Absorption↗
PubMed1986

Prefeeding-dependent anaerobic metabolization of xenobiotics by intestinal bacteria--methods for acarbose metabolites in an artificial colon.

The biotransformation of Acarbose (Bay g 5421) by an artificial in vitro system with viable intestinal microorganisms was investigated. The bacteria were obtained from the colon of man or from the caecum and colon of rats and were incubated anaerobically with 14C-Acarbose in a nutrient solution. The metabolites were separated and purified by chromatographic methods and identified by nuclear magnetic resonance (1H; 13C) spectrometry and by mass spectrometry. Metabolites in man and rat are component 2 (minus the terminal glucose of Acarbose), a basic disaccharide consisting of rings B and C, and component 1. This latter substance is formed, after hydrolytic cleavage of the internal glucose of Acarbose, by spontaneous rearrangement of rings A and B (Acarviosine) into a tricyclic oxazolidine. The metabolite pattern of Acarbose is changed profoundly after several weeks of pretreatment of man or rat with this compound. The microflora adapted in such a manner yields in addition methylated, hexosylated, and n-butyroylated derivatives of Acarbose and/or component 2.

Acarbose↗
PubMedDate not supplied

Multicenter, randomized, controlled trial of heat-killed Lactobacillus acidophilus LB in patients with chronic diarrhea.

Chronic diarrhea is a common bowel disorder; disturbance of intestinal microorganisms may play a role in its pathogenesis. This study assessed the clinical efficacy of lyophilized, heat-killed Lactobacillus acidophilus LB versus living lactobacilli in the treatment of chronic diarrhea. One hundred thirty-seven patients with chronic diarrhea were randomly allocated to receive either a 4-week course of 2 capsules of Lacteol Fort twice a day (Lacteol group, 69 patients) or a 4-week course of 5 chewable tablets of Lacidophilin three times a day (Lacidophilin group, 64 patients). The frequency of stools was recorded quantitatively, and semiquantitative parameters such as stool consistency, abdominal pain, distention, and feeling of incomplete evacuation were evaluated. At the second and fourth week of treatment, mean bowel frequency was significantly lower in the Lacteol group than in the Lacidophilin group (1.88 +/- 1.24 vs 2.64 +/- 1.12, 1.39 +/- 0.92 vs 2.19 +/- 1.05; P<.05). At the end of the treatment, the clinical symptoms were markedly improved in the Lacteol group, indicating that L. acidophilus LB is more effective than living lactobacilli in the treatment of chronic diarrhea.

Adolescent↗
PubMed2003

Differential effect of bovine serum albumin on ginsenoside metabolite-induced inhibition of alpha3beta4 nicotinic acetylcholine receptor expressed in Xenopus oocytes.

Ginsenosides, major active ingredients of Panax ginseng, that exhibit various pharmacological and physiological actions are transformed into compound K (CK) or M4 by intestinal microorganisms. CK is a metabolite derived from protopanaxadiol (PD) ginsenosides, whereas M4 is a metabolite derived from protopanaxatriol (PT) ginsenosides. Recent reports shows that ginsenosides might play a role as pro-drugs for these metabolites. In present study, we investigated the effect of bovine serum albumin (BSA), which is one of major binding proteins on various neurotransmitters, hormones, and other pharmacological agents, on ginsenoside Rg2-, CK-, or M4-induced regulation of alpha3beta4 nicotinic acetylcholine (ACh) receptor channel activity expressed in Xenopus oocytes. In the absence of BSA, treatment of ACh elicited inward peak current (I(ACh)) in oocytes expressing alpha3beta4 nicotinic ACh receptor. Co-treatment of ginsenoside Rg2, CK, or M4 with ACh inhibited I(ACh) in oocytes expressing (alpha3beta4 nicotinic ACh receptor with reversible and dose-dependent manner. In the presence of 1% BSA, treatment of ACh still elicited I(ACh) in oocytes expressing alpha3beta4 nicotinic ACh receptor and co-treatment of ginsenoside Rg2 or M4 but not CK with ACh inhibited I(ACh) in oocytes expressing alpha3beta4 nicotinic ACh receptor with reversible and dose-dependent manner. These results show that BSA interferes the action of CK rather than M4 on the inhibitory effect of I(ACh) in oocytes expressing alpha3beta4 nicotinic ACh receptor and further suggest that BSA exhibits a differential interaction on ginsenoside metabolites.

Acetylcholine↗
PubMed2001

Polyamines in cell growth and cell death: molecular mechanisms and therapeutic applications.

Polyamines are aliphatic cations with multiple functions and are essential for life. Cellular polyamine levels are regulated by multiple pathways such as synthesis from amino acid precursors, cellular uptake mechanisms that salvage polyamines from diet and intestinal microorganisms, as well as stepwise degradation and efflux. Investigations using polyamine biosynthetic inhibitors indicate that alterations in cellular polyamine levels modulate normal and cancer cell growth. Studies using transgenic mice overexpressing polyamine biosynthetic enzymes support a role of polyamines in carcinogenesis. Many, if not all, signal transduction pathways intersect with polyamine biosynthetic pathways and the regulation of intracellular polyamine levels. Direct binding of polyamines to DNA and their ability to modulate DNA-protein interactions appear to be important in the molecular mechanisms of polyamine action in cell proliferation. Consistent with the role of polyamines as facilitators of cell growth, several studies have shown their ability to protect cells from apoptosis. However, polyamines also have a role in facilitating cell death. The basis of these diverse cellular responses is currently not known. Cell death response might be partly mediated by the production of hydrogen peroxide during polyamine catabolism. In addition, the ability of polyamines to alter DNA-protein and protein-protein interactions might be disruptive to cellular functions, when abnormally high levels are accumulated due to defects in polyamine catabolic or efflux pathways. A large body of data indicates that polyamine pathway can be a molecular target for therapeutic intervention in several types cancers. Inhibitors of biosynthesis, polyamine analogues as well as oligonucleotide/polyamine analogue combinations are promising drug candidates for chemoprevention and/or treatment of cancer.

Animals↗
PubMed1997

The urinary excretion of arsenic metabolites after a single oral administration of dimethylarsinic acid to rats.

The biotransformation following oral administration of dimethylarsinic acid (DMA), an organoarsenical herbicide and the main metabolite of inorganic arsenic in mammals, was studied in rats. Male F344/DuCrj rats were administered a single dose of DMA (50 mg/kg) orally. Urine was collected at 0, 2, 4, 8, 10, 24, and 48 h after administration by forced urination. Arsenic metabolites in urine were analyzed by ion chromatography with inductively coupled plasma mass spectrometry (IC-ICP-MS). The proportions of urinary elimination of DMA, trimethylarsine oxide (TMAO), methylarsonic acid (MMA), an unidentified arsenic metabolite, and arsenite were determined at various timepoints after administration. Unmetabolized DMA was the most common form excreted during the first 4 h. Thereafter, a gradual decrease in the proportion of DMA was observed, while progressive increases in those of TMAO, the unidentified metabolite, and arsenite occurred. The proportion of TMAO excreted amounted to over 50% of all arsenic in urine between 6 and 24 h. The proportion of the unidentified metabolite and arsenite were each approximately 10% at 10 and 24 h after administration. The findings indicate that DMA administered to rats was initially excreted as unchanged DMA, and later as the methylated metabolite, TMAO. Arsenite, a demethylated metabolite of DMA, also was excreted later than elimination of DMA and TMAO. The hypothesis of demethylation by intestinal microorganisms can be supported by comparing the metabolites following oral and intraperitoneal administration. The unidentified metabolite was readily decomposed by HCl but was left unchanged by NaOH; these findings suggest that it was present in a complexed form in urine.

Administration, Oral↗
PubMed1985

The presence of 5 alpha-sitostanol in the serum of a patient with phytosterolemia, and its biosynthesis from plant steroids in rats with bile fistula.

The presence of 5 alpha-sitostanol (24-ethyl-5 alpha-cholestan-3 beta-ol) in serum of a patient with the rare genetic disease phytosterolemia was confirmed. This study aimed at clarifying the pathway(s) for the formation of 5 alpha-sitostanol, by use of rats with bile fistula. 5 alpha-Sitostanol was formed only slowly from sitosterol, but readily from 24-ethyl-4-cholesten-3-one. Some conversion was also obtained with 7 alpha-hydroxysitosterol as precursor. In view of the low rate of 7 alpha-hydroxylation of sitosterol, however, a pathway from sitosterol to 5 alpha-sitostanol involving 7 alpha-hydroxysitosterol as intermediate is probably of small physiological importance. Intestinal microorganisms are not essential for the above conversions, since the 5 alpha-sitostanol was found in bile from bile fistula rats. 5 alpha-Sitostanol was converted to water soluble metabolites (bile acids) much more slowly than was cholestanol (5 alpha-cholestan-3 beta-ol), and was accumulated serum to a much larger extent.

Adolescent↗
PubMed1985

Biliary excretion and enterohepatic circulation of 1-nitropyrene metabolites in Fischer-344 rats.

1-Nitropyrene (1-NP), present in diesel engine emissions, is a potent mutagen to bacteria, such as those found in mammalian intestinal tract, which contain nitroreductase enzymes. The purposes of this study were to determine the importance of bile as a route of excretion of 1-NP metabolites and to determine if reabsorption of biliary metabolites required the presence of intestinal bacteria. The bile ducts of male Fischer-344 rats were cannulated, 0.3 or 1.2 mumoles [3H]1-NP was given i.v., and bile, urine, and feces were collected for 24 hr. Biliary excretion accounted for 70 (80%) or 170 (60%) nmoles of [3H]1-NP after the low and high dose, respectively, with half-times for excretion of 1.7 hr +/- 0.3 (+/- S.E.M.) and 3.4 hr +/- 1.6 (+/- S.E.M.). Excretion of [3H]1-NP equivalents in the urine was linearly related to dose, with 6 or 16 nmoles (8%) excreted in 24 hr. At the low dose, more radioactivity appeared in the urine in control rats compared to bile-duct cannulated rats, suggesting that reabsorption of 1-NP metabolites occurred. Pretreatment of rats with orally administered antibiotics prior to i.v. injection of 0.3 mumole [3H]1-NP decreased radioactivity excreted in urine compared to untreated controls, suggesting that intestinal microorganisms may alter the biliary metabolites of 1-NP to facilitate reabsorption. Pretreatment of rats with buthionine sulfoximine, a glutathione depletor, decreased the excretion of certain biliary metabolites, suggesting that they were mercapturic acids of 1-NP metabolites. In summary, the results of these studies indicate that bile was an important route of excretion of nitropyrene metabolites. A portion of the excreted metabolites was reabsorbed from the gut, and this reabsorption required the presence of gut microorganisms.

Animals↗
PubMed1986

Bacterial contamination of pancreatic necrosis. A prospective clinical study.

In a prospective clinical study including 114 patients with acute necrotizing pancreatitis, but excluding patients with a pancreatic abscess, necrotic material obtained at surgery was tested bacteriologically. Intestinal microorganisms were cultured in 39.4% of the cases. The contamination rate was 23.8% in patients operated on during the first 7 days of the attack; it rose to 71.4% in the third week and decreased to 32.5% after the fourth week. Intra- and extrapancreatic necrosis was more widespread and pancreatitis-associated ascites was more frequent in patients with proven contamination. The number of objective signs was 4.5 (median) and postoperative mortality was 37.8% in bacteriologically positive subjects, whereas the number was 3.5 (median) and mortality was 8.7% in bacteriologically negative patients. Morphologic and clinical alterations were more severe, and the mortality rate was significantly elevated, in patients with a short history of disease and bacterial contamination of necrotic tissue. All 5 patients with pancreatic sepsis who were operated on in the first 7 days of the disease, as compared with 2 of 16 patients with sterile necrosis, died. Thus, it is demonstrated that bacterial contamination of pancreatic necrosis occurs early and frequently, causing a significant increase in morbidity and mortality, particularly when it develops in the initial stages of the attack.

Abscess↗
PubMed1986

Metabolism and DNA binding of 2,6-dinitrotoluene in Fischer-344 rats and A/J mice.

2,6-Dinitrotoluene (2,6-DNT) is a potent hepatocarcinogen in Fischer-344 rats, while its 2,4-isomer is believed to be noncarcinogenic. Neither 2,6-DNT nor 2,4-DNT is carcinogenic in the strain A mouse lung tumor bioassay. To explore the possible reasons for these differences in tumor responses, we have studied the in vitro metabolism and DNA binding of 2,6-DNT in cultured hepatocytes of the Fischer-344 rat and the A/J mouse, and have also investigated the in vivo DNA binding of 2,6-DNT and 2,4-DNT in these two species. In vitro metabolism of 2,6-DNT by rat and mouse hepatocytes was similar and resulted mainly in the formation of 2,6-dinitrobenzyl alcohol, either unconjugated or as a glucuronide (57.5 to 85.5% of the total per fraction), with smaller amounts of polar, acidic metabolites (8.4 to 38.7%) and minor amounts (1.2 to 5.3%) of 2-amino-6-nitrotoluene. Anaerobic metabolism of 2,6-DNT by an extract of rat or mouse cecal contents resulted mainly in the formation of 2-amino-6-nitrotoluene and 2-(N-acetylamino)-6-nitrotoluene, and minor amounts of 2,6-diaminotoluene. Ip administration of 2,6-DNT or 2,4-DNT (150 mg/kg each) to Fischer-344 rats resulted, after 24 hr, in covalent binding to DNA of the liver (131.1 to 259.9 pmol 2,6-DNT/mg DNA; 215.4 to 226.8 pmol 2,4-DNT/mg DNA), and lower binding to DNA of the lungs and the intestine (14.9 to 22.7 pmol 2,6-DNT/mg DNA; 45.0 to 75.0 pmol 2,4-DNT/mg DNA). Similar treatment of A/J mice resulted in lower binding in the liver (25.9 to 31.9 pmol 2,6-DNT/mg DNA; 42.6 to 58.9 pmol 2,4-DNT/mg DNA), no detectable binding of 2,6-DNT in extrahepatic tissues and low amounts of binding of 2,4-DNT to lung and intestinal DNA (9.7 to 39.0 pmol/mg DNA). In vitro binding of 2,6-DNT to DNA of cultured hepatocytes from both A/J mice and Fischer-344 rats required prior metabolism of 2,6-DNT by the respective extracts from cecal contents. DNA binding was non-detectable in hepatocytes incubated with 2,6-DNT only. It is concluded that binding of 2,6-DNT to liver DNA requires its prior reductive metabolism, probably by intestinal microorganisms, and that the higher binding of 2,6-DNT in the Fischer-344 rat than in the A/J mouse may, in part, be responsible for the high susceptibility of the Fischer-344 rat to 2,6-DNT carcinogenesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Expression of the bile acid-inducible NADH:flavin oxidoreductase gene of Eubacterium sp. VPI 12708 in Escherichia coli.

The intestinal microorganism Eubacterium sp. VPI 12708 synthesizes a bile acid-inducible NADH:flavin oxidoreductase (NADH:FOR) which presumably functions in the 7 alpha-dehydroxylation of cholic acid to deoxycholic acid. The baiH gene encoding NADH:FOR was subcloned into an IPTG-inducible expression vector, pBaiH2.2. Escherichia coli DH5 alpha cells transformed with pBaiH2.2 expressed 10-fold higher levels of NADH:FOR upon induction with IPTG than did Eubacterium sp. VPI 12708 cells induced with cholic acid. The NADH:FOR produced by E. coli DH5 alpha(pBaiH2.2) was purified to > 95% electrophoretic homogeneity in three steps. The purified NADH:FOR was similar to that of Eubacterium sp. VPI 12708 in subunit and native M(r) (ca. 72,000 and 210,000, respectively), pH optimum, sensitivity to inhibitors, and electron acceptor specificity. It contained 1 mol of FAD, up to 2 mol of iron, and 1 mol of copper per mol of subunit. The enzyme reduced synthetic quinones, dyes, flavins, and O2 with NADH as the electron donor, but did not reduce disulfide compounds, various unsaturated bile acids, cytochrome c, physiological quinones, or cell fractions from Eubacterium sp. VPI 12708. Addition of purified NADH:FOR to Eubacterium sp. VPI 12708 cell extracts altered the balance of oxidized and reduced bile acid intermediates produced during cholic acid 7 alpha-dehydroxylation, suggesting that the enzyme may regulate the cellular ratio of NAD to NADH.

Amino Acid Sequence↗