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PubMed1999

Ivermectin in reindeer feces: determination by HPLC.

An assay method for the determination of ivermectin in reindeer feces was developed. Ivermectin was quantified by high-performance liquid chromatography and fluorescence detection after extraction (acetone, isooctane), cleanup (C-18 solid-phase extraction column), and derivatization to a fluorescent derivative using N-methylimidazole and trifluoroacetic anhydride. Concentration calculations were based on calibration lines found from analyses of standards prepared in feces. Abamectin was used as internal standard. Ivermectin was determined over a wide concentration range in a single sample preparation and HPLC run for each sample. The recovery from fortified samples was greater than 95% over the concentration range 5-2000 ng/g wet weight feces.

Animals↗
PubMed2001

High prevalence of TT virus in human bile juice samples: importance of secretion through bile into feces.

TT virus (TTV) is much more prevalent than we once imagined. With the use of primers designed from the noncoding regions, a more than 90% rate of TTV infection in the general population by polymerase chain reaction (PCR) has been reported, showing that nonparenteral transmission must play an important role to its epidemiology. We considered that TTV may be secreted through bile juice into feces to establish nonparenteral infection. Paired bile juice and serum samples were obtained from 26 patients who were receiving bile drainage. Feces were also recovered after the drainage tube was removed. TTV DNA was detected from 22 patients in serum (84.6%), and they were all TTV DNA positive in bile juice. Most feces samples recovered from TTV-positive patients were also TTV DNA positive. Secretion of TTV into bile juice appears to be common, and this could play an important role to its transmission and its epidemiology.

Bile↗
PubMed1999

Influence of feces from patients with ulcerative colitis on butyrate oxidation in rat colonocytes.

An impaired oxidation of butyrate has been suggested as a causative factor of ulcerative colitis and, moreover, agents present in colonic luminal contents impair butyrate oxidation in both rat and human colonocytes. To evaluate the overall effect of feces on the production of CO2 and ketone bodies from butyrate oxidation in rat colonocytes, fecal homogenates from 10 healthy subjects and 10 patients with quiescent and 10 patients with active ulcerative colitis were sterile filtrated and added to rat colonocytes incubated with 2, 4, and 10 mmol/liter of stock butyrate, respectively. Addition of fecal filtrate from healthy subjects and patients with quiescent and active ulcerative colitis to colonocytes incubated with 2, 4, and 10 mmol/liter of stock butyrate, respectively, tended to decrease the production of CO2 from butyrate oxidation, whereas ketogenesis was unaffected. The decrease in CO2 production was not explained by the simultaneous addition of fecal short-chain fatty acids (SCFAs). However, a difference in the ability to decrease CO2 production was not found between filtrates from healthy subjects and patients with quiescent and active ulcerative colitis. In conclusion, feces from healthy subjects and patients with quiescent and active ulcerative colitis contain inhibitor(s) of the production of CO2 from butyrate oxidation in colonocytes. However, a specific inhibitory effect of feces from patients with ulcerative colitis on the production of CO2 could not be identified.

Adult↗
PubMedDate not supplied

Partitioning of polybrominated biphenyls (PBBs) in serum, adipose tissue, breast milk, placenta, cord blood, biliary fluid, and feces.

Polybrominated biphenyl (PBB) concentrations in specimens from adult males and females were used to determine the distribution of PBBs in body tissues and the partitioning ratio between types of tissues. Specimens of serum, adipose tissue, biliary fluid, and feces were tested by gas chromatography. In addition, parturient women provided breast milk, placenta, and cord blood for testing. There was a significant correlation between serum and adipose PBB levels. Pregnant and nonpregnant women and male chemical workers had similar serum to adipose tissue concentration ratios, which ranged from 1:140 to 1:260. Males from farms had a significantly different ratio of 1:325-329. Potential exposure to the fetus and newborn was demonstrated. Cord blood contained one-tenth of the concentration found in maternal serum which indicated partial placental passage. Human milk contained PBBs at 107 to 119 times the quantity found in maternal serum. Polybrominated biphenyls were detectable in bile and feces demonstrating transfer into the intestinal tract. The concentration of PBBs in feces represented a minor proportion of the total body burden indicating a slow rate of excretion.

Adipose Tissue↗
PubMed1998

Detection of Helicobacter pylori gene by means of immunomagnetic separation-based polymerase chain reaction in feces.

BACKGROUND: Detection of Helicobacter pylori is usually performed by culture, polymerase chain reaction (PCR), histology, or urease test on gastric biopsy samples. Although methods based on feces are non-invasive, their sensitivity has been relatively low. In this study, to improve its sensitivity, immunomagnetic separation (IMS) was used as a pre-PCR step for direct detection of H. pylori in feces. METHODS: Fresh fecal samples were taken from 72 patients attending for endoscopy. Of these, 57 patients had a positive H. pylori status according to the results of culture, histology, and PCR on gastric biopsy samples. Anti-H. pylori antibody-sensitized immunomagnetic beads were used to concentrate the bacteria. PCR was then performed to detect the H. pylori urease A-encoding gene. RESULTS: Of the 57 H. pylori-positive patients, 35 (61.4%) had positive fecal samples by IMS-based PCR method. None of the 15 H. pylori-negative patients had positive fecal samples. The sensitivity of this method was 61.4%, and the specificity 100.0%. CONCLUSIONS: This study confirms that non-invasive diagnosis of H. pylori infection could be made from feces by using IMS-based PCR.

Feces↗
PubMed2005

Excretion of living Borrelia recurrentis in feces of infected human body lice.

Louse-borne relapsing fever (LBRF), caused by Borrelia recurrentis, is 1 of the most dangerous arthropod-borne diseases. Infection is thought to occur through louse crushing. Lice feces have not been shown to contain living borreliae. We infected 800 body lice by feeding them on a rabbit made spirochetemic by the injection of 2 x 106 borreliae. The life span of infected lice was not shortened. Once infected, lice remained infected for life but did not transmit borreliae to their progeny or to nurse rabbits. B. recurrentis infection was observed throughout lice and spread into hemolymph on day 5 after infection. We describe 2 unprecedented phenomena. In hemolymph, B. recurrentis formed clumps of aggregated borreliae. Using immunofluorescence assay, transmission electron microscopy, and culture, we detected borreliae excreted in lice feces beginning on day 14 after infection. We conclude that, similar to epidemic typhus and trench fever, transmission of LBRF may be caused by lice feces.

Animals↗
PubMed1980

Characterization of a mutagenic bacterial product in human feces.

Mutagens detectable with the Ames assay have been found in the feces of apparently healthy individuals and the incidence of this mutagenic activity was found to be greater in a population at high risk for colon cancer than in a population at low risk. A compound accounting for the mutagenic activity has been isolated by high performance liquid chromatography. Two closely related forms which behave identically chemically could be resolved. The compound was active on Salmonella typhimurium TA98 and TA100, had a characteristic ultraviolet absorption spectrum with maxima at about 320, 340, and 365 nm, fluoresced green in long wavelength ultraviolet light, and had the same mobility on the thin-layer chromatography as the mutagenic activity in a direct ether extract of feces. The compound was unstable in air but could be stabilized in the presence of butylated hydroxytoluene. Upon oxidation the compound lost its mutagenicity and its ultraviolet absorption spectrum underwent a blue shift so that the absorption maxima were at 295, 310, and 325 nm. Determination of the structure of the mutagen has been difficult since the compound was not volatile and production of a volatile derivative has not been successful. On thin-layer chromatography plates the compound reacted with reagents that detect chlorinated compounds. By thermal energy analysis it did not appear to contain a nitroso group. The compound increased in concentration upon anaerobic incubation of feces at 37 C and this increase was prevented by cold, air, and antimicrobial agents. This suggests to us that the fecal flora produces the compound.

Bacteria↗
PubMed1982

Monitoring N-nitrosamino acids excreted in the urine and feces of rats as an index for endogenous nitrosation.

A simple and sensitive method for the quantitative estimation of endogenous N-nitrosation in rats has been developed. This approach is based on the findings that N-nitrosamino acids (e.g., nitrosoproline (NPRO), nitrosohydroxyproline (NHPRO) and nitrososarcosine (NSAR)) when administered orally to rats, are excreted unchanged almost quantitatively (88-96% of the dose) in the urine and feces. After sequential administration of a nitrosatable amino acid and sodium nitrite the nitrosamino acid excreted in the urine and feces was analyzed. The amount of NPRO excreted in the urine of rats was proportional to the dose of proline and to the square of the nitrite dose. Co-administration of ascorbic acid and alpha-tocopherol together with the precursors decreased the urinary NPRO whereas thiocyanate increased the yield. After feeding an amino acid precursor and nitrite, the yield of nitrosamino acids formed in vivo and excreted in the urine increased in the order: NPRO less than NSAR less than NHPRO. The same order was seen when the nitrosation rates of the amino acids in vitro were compared. Thus N-nitrosation in vivo in rats occurs via a similar mechanism as observed in vitro. Monitoring of N-nitrosamino acids excreted in the urine and feces thus appears to provide a valuable index for endogenous N-nitrosation.

Amino Acids↗
PubMed1975

Absence of hepatitis B antigens from feces and sewage as a result of enzymatic destruction.

Hepatitis B surface antigen (HBs Ag) was not detected in sewage by means of a sensitive affinity chromatography method combined with radioimmunoassay. The antigen was also absent from the feces and urine of 23 patients with HBs Ag antigenemia; this observation indicates that HBs Ag is rarely discharged into sewage. The absence of HBs Ag from feces is ascribed to antagonists of an enzymatic nature or to carboxypeptidase A, which destroys the antigen. Antagonists with similar effects were produced by three species of Pseudomonas but were not produced by various other bacteria. HBs Ag was also destroyed by two subtilisin enzymes. When hepatitis B sera were incubated with these enzymes or with the antagonists, small spherical particles, tubules, and the coats of Dane particles disappeared first, and Dane cores disappeared later. Although sewage or activated sludge did not affect the stability of HBs Ag, the results indicate that even Dane cores are not excreted in feces and that sewage plays a negligible role in the spread of HBs Ag, Dane cores, and viral hepatitis type B.

Bacteriological Techniques↗
PubMed1977

Characterization of Toxoplasma gondii from the feces of naturally infected cats.

Feces of 1,000 cats from a humane shelter in Columbus, Ohio, were examined microscopically for oocysts of Toxoplasma gondii and by inoculation into mice. From the first 541 cats examined, oocysts of Toxoplasma were found in the feces of seven cats but in none of the remaining 459 cats. Results of the dye test in these seven cats showed titers of antibody of less than 1:2 in four cats, and of 1:8, 1:6, and 1:32 in the remaining three cats. The pathogenicity and infectivity of oocysts and cysts of all seven strains were compared in mice after oral and intraperitoneal inoculations. Oocysts and cysts were more pathogenic when administered by the oral route than by the intraperitoneal route. The cysts were less pathogenic than the oocysts. Excellent cross-immunity between six of these seven feline strains and the M-7741 strain was deomonstrated in cats by the fact that oocysts were not shed in feces of cats challenged with cysts of homologous or heterologous strains.

Animals↗
PubMed1984

Effects of dietary calcium and fat on cholesterol in tissues and feces of young goats.

To examine the effects of amount of calcium and type of fat in the diet on distribution of cholesterol in plasma, several tissues and feces, 4-week-old goats (6 females and 18 males) were fed isocaloric diets consisting of goat milk supplemented with cholesterol and 1) soybean oil, 2) tallow, 3) soybean oil and CaCO3 or 4) tallow and CaCO3 for 20 weeks. Plasma cholesterol increased initially in all animals; plasma and lipoprotein cholesterol concentrations, however, were not affected by dietary fat or calcium. Goats fed CaCO3 excreted more calcium and ash in their feces and had greater cholesterol and fat concentrations in their livers. Neutral steroid, but not bile acid, excretion was greater in soybean oil-fed goats than in goats fed tallow. Soybean oil-fed goats had greater cholesterol concentrations in the viscera (minus liver) and tended to have greater cholesterol concentrations in the carcass and whole body. Aortas of soybean oil-fed goats exhibited greater fat deposition. In summary, dietary fat, but not calcium, significantly altered cholesterol disposition in young goats by affecting cholesterol deposition in tissues and excretion in feces, without a concomitant change in plasma cholesterol.

Absorption↗
PubMed1998

Pharmacokinetics of soybean isoflavones in plasma, urine and feces of men after ingestion of 60 g baked soybean powder (kinako).

To take advantage of the various pharmacologic activities of soy bean isoflavones, more detailed studies of the absorption and excretion rates of these compounds in humans and subsequent evaluation of their bioavailabilities are required. We conducted a pharmacokinetic study of soybean isoflavones in seven healthy male volunteers. After ingestion of 60 g of kinako (baked soybean powder, containing 103 micromol daidzein and 112 micromol genistein), changes of the isoflavone and metabolite concentrations in plasma, urine and feces were measured by gas chromatography-mass spectrometry. The plasma concentration of genistein increased after 2 h and reached its highest value of 2.44 +/- 0.65 micromol/L 6 h later. The plasma concentration of daidzein peaked at 1.56 +/- 0.34 micromol/L at the same time, but it was always lower than that of genistein. Peak plasma concentration of O-desmethylangolensin (O-DMA) and equol appeared after the daidzein peak in four and two subjects, respectively. In contrast with plasma, daidzein was the main component in urine. Urinary daidzein excretion started to increase shortly after the rise in its plasma concentration and reached 2.4 micromol/h 8 h after ingestion of kinako. Genistein excretion in urine paralleled that of daidzein, but the value at 6 h was about half (1.1 micromol/h). The majority of ingested isoflavones after ingestion of kinako were recovered on d 2 or 3 in the feces. Total recovery of daidzein, O-DMA and equol from urine and feces was 54.7%, calculated from daidzein intake; 20.1% of administered genistein was recovered as genistein. The half-lives of plasma genistein and daidzein were 8.36 and 5.79 h, respectively. The individual plasma and urinary concentrations of equol and O-DMA were quite variable; subjects were classified as high and low metabolizers. The high plasma concentration of isoflavones for at least several hours after a single ingestion of soy protein suggests that these compounds may interact with macromolecules and have biological effects.

Absorption↗
PubMed2004

Supplementation of a diet low in carotenoids with tomato or carrot juice does not affect lipid peroxidation in plasma and feces of healthy men.

Antioxidant properties of carotenoids are thought to be at least partly responsible for the protective effects of fruits and vegetables rich in carotenoids against colon cancer. There are large amounts of in vitro data supporting this hypothesis. But there is little known about the antioxidant effects of carotenoid-rich food in vivo particularly in the gastrointestinal tract. In a randomized, crossover trial, healthy men (n = 22) who were consuming a low-carotenoid diet drank 330 mL/d tomato juice or carrot juice for 2 wk. Antioxidant capacity was assessed by the "lag time" of ex vivo LDL oxidation induced by copper and lipid peroxidation as determined by measurements of malondialdehyde (MDA) in plasma and feces using HPLC with fluorescence detection. Although consumption of both carotenoid-rich juices for 2 wk increased the carotenoid level in plasma and feces (P < 0.001), the antioxidant capacity of LDL tended to be increased by only approximately 4.5% (P = 0.08), and lipid peroxidation in the men's plasma and feces was not affected. Thus, processes other than lipid peroxidation could be responsible for the preventive effects of tomatoes and carrots against colon cancer.

Antioxidants↗
PubMed1980

Effects of cholic acid, chenodeoxycholic acid, and their related bile acids on cholesterol, phospholipid, and bile acid levels in serum, liver, bile, and feces of rats.

Effects of sodium cholate, deoxycholate, chenodeoxycholate, and lithocholate on serum and liver cholesterol levels, bile flow, biliary cholesterol, phospholipids, and bile acids, and fecal sterols and bile acids were examined in Wistar strain male rats fed either an ordinary diet or a 2% cholesterol diet. Cholate and deoxycholate increased serum and liver cholesterol levels, serum pre beta-lipoprotein, bile flow, and biliary secretion of cholesterol, phospholipids, and bile acids, but chenodeoxycholate and lithocholate did not. The total amounts of sterols and of bile acids in the feces did not differ between the cholate and the chenodeoxycholate groups. All the bile acids except lithocholate decreased fecal coprostanol when the diet included cholesterol. Cholate and deoxycholate produced similar bile acid compositions in the bile and feces, as was the case between chenodeoxycholate and lithocholate, though chenodeoxycholate slightly increased the amount of muricholic acids, and lithocholate that of hyodeoxycholic acid, in the feces. The effects of cholate and deoxycholate are similar to each other but different from that of chenodeoxycholate or lithocholate in rats. Cholate causes marked accumulation of cholesterol in tissues, increased bile flow and biliary lipid secretion but chenodeoxycholate does not. Cholate is absorbed much more efficiently than chenodeoxycholate.

Animals↗
PubMed1986

Bile alcohol profiles in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis.

Bile alcohols in bile, urine, and feces of a patient with cerebrotendinous xanthomatosis have been analyzed by a combination of capillary gas-liquid chromatography and mass spectrometry after fractionation into groups according to mode of conjugation. The presence of at least 18 bile alcohols, which were excreted mainly as glucurono-conjugates in bile and urine, and as unconjugated forms in feces, was demonstrated. The following bile alcohols were identified with certainty by direct comparison with reference compounds: 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol; (23R)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,23-tetrol; 5 alpha- and 5 beta-cholestane-3 alpha,7 alpha,12 alpha,24-tetrols; 5 alpha- and 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25-tetrols; 27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentol; (22R)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,22,25-pentol; (23R)- and (23S)-5 beta-cholestane-3 alpha,7 alpha, 12 alpha,23,25-pentols; 3 alpha,12 alpha,25-trihydroxy-5 beta-cholestane-7-one; (24R)- and (24S)-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentols; 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25,26-pentol. Although the bile alcohol profile in urine was quite different from those in bile and feces, the determination of urinary bile alcohols as well as of biliary and fecal bile alcohols could be used for diagnosis of cerebrotendinous xanthomatosis.

Adult↗
PubMed1979

Carcinoembryonic antigen (CEA) in gastric juice or feces as an aid in the diagnosis of gastrointestinal cancer.

Carcinoembryonic antigen (CEA) levels in the feces and serum were evaluated in 22 colorectal cancer patients and 20 healthy volunteers; in CEA levels gastric juice and serum were also evaluated in 28 gastric cancer patients and 14 peptic ulcer patients. Fecal CEA was found in all of 22 colorectal cancer patients as well as in the 20 healthy volunteers. Elevated fecal CEA levels were observed in the colorectal cancer patients, as compared to the healthy volunteers. The feces of 15 of the 22 colorectal cancer patients contained CEA at concentrations higher than the mean value plus twice the standard deviation of the healthy volunteers. The fecal CEA levels did not correlate directly either with Dukes' stage or serum CEA levels. CEA in gastric juice was elevated significantly in 26 of gastric cancer patients, with the exception of two patients with early gastric cancer. On the other hand, serum CEA was elevated in only nine of the 28 gastric cancer patients. These results point out the distinct value of assaying CEA in the feces or gastric juice as an aid in the diagnosis of colorectal or gastric cancer.

Adult↗
PubMed1988

The role of feces, necrotic tissue, and various blocking agents in the prevention of adhesions.

Ischemic tissue and intraperitoneal bacteria have been ascribed an etiologic role in the production of intra-abdominal adhesions. To further elucidate the role of these stimuli and to evaluate the potential protective effect of various agents, peritonitis was induced in 160 Sprague-Dawley rats. The experiment was stratified into those animals with peritonitis plus necrotic tissue, solid feces, both, or neither. The agents tested were a nonsteroidal anti-inflammatory (ibuprofen), free radical scavenger (SOD), and an anticoagulant (heparin). Death was less likely to occur in animals treated with heparin (3 of 40 vs. 12 of 40, p less than 0.01) or SOD (4 of 40 vs. 12 of 40, p less than 0.05). Ibuprofen did not increase survival in this model. Heparin protected against adhesions in animals with an ischemic ileum of limb and without solid feces. In animals with a nonischemic isolated segment of ileum and solid feces, adhesion formation was increased in both the ibuprofen and the heparin treatment groups (p less than 0.05).

Animals↗
PubMed2001

Gas production by feces of infants.

BACKGROUND: Intestinal gas is thought to be the cause abdominal discomfort in infants. Little is known about the type and amount of gas produced by the infant's colonic microflora and whether diet influences gas formation. METHODS: Fresh stool specimens were collected from 10 breast-fed infants, 5 infants fed a soy-based formula, and 3 infants fed a milk-based formula at approximately 1, 2, and 3 months of age. Feces were incubated anaerobically for 4 hours at 37 degrees C followed by quantitation of hydrogen (H2), methane (CH4), carbon dioxide (CO2), hydrogen sulfide (H2S), methanethiol (CH3SH), and dimethyl sulfide (CH3SCH3) in the head-space. RESULTS: H2 was produced in greater amounts by breast-fed infants than by infants in either formula group, presumably the consequence of incomplete absorption of breast milk oligosaccharides. CH4 was produced in greater amounts by infants fed soy formula than by infants on other diets. CO2 was produced in similar amounts by infants in all feeding groups. Production of CH3SH was conspicuously low by feces of breast-fed infants and production of H2S was high by soy-formula-fed infants. CH3SCH3 was not detected. Only modest changes with age were observed and there was no relation between gas production and stool consistency, although stools were more likely to be malodorous when concentrations of H2S and/or CH3SH were high. CONCLUSIONS: Gas release by infant feces is strongly influenced by an infant's diet. Of particular interest are differences in production of the highly toxic sulfur gases, H2S and CH3SH, because of the role that these gases may play in certain intestinal disorders of infants.

Carbon Dioxide↗