Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:036187 (gut)
 73,132 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve marmosets (Saguinus mystax) were inoculated intravenously (iv) with hepatitis A virus (HAV). One died early (day 12); seven were sacrificed at the time of elevation in level of alanine aminotransferase (serum glutamic-pyruvic transaminase), and four without elevation were not sacrificed but seroconverted. In the seven marmosets sacrificed during the acute stage of illness, hepatitis A antigen (HA Ag) was detected in the liver by immunofluorescence in all cases, by immune electron microscopy in four, and by enzyme-linked immunosorbent assay (ELISA) in three. The HA Ag appeared by immunofluorescence as very fine granules in the cytoplasm of hepatocytes and Kupffer cells. The HA Ag could not be detected by immunofluorescence in biopsy specimens taken from the duodenum, jejunum, ileum, or transverse colon in any of eight marmosets in which necropsy was performed during the acute or preacute stage of illness. These findings suggest that the gut is not involved during the acute phase of HAV infection following iv inoculation into marmosets. The ELISA results showed that only three of 12 marmoset livers obtained during the acute phase of HAV infection could be used as an antigen source in serologic testing for antibody to HA Ag. Thus, marmoset livers were no better as a source of HA Ag than acute-phase stools from patients with type A hepatitis.
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PMID:Localization of hepatitis A antigen in marmoset organs during acute infection with hepatitis A virus. 21 88

The rosy barb (Puntius conchonius) was exposed to copper (Cu) for short (48 hr) and long (8 weeks) terms and effects on enzyme activities and biochemical variables in the blood and tissues were examined. In vivo exposure to 571 micrograms CuSO4/liter (96-hr median tolerance limit (TLm)) for 48 hr stimulated to varying degrees acid phosphatase (AcP), alkaline phosphatase (AlP) (except in the liver), and acetylcholinesterase activities in selected tissues. The alanine aminotransferase and lactic dehydrogenase (LDH) (except in the heart) activities were inhibited to varying degrees in vivo. In vitro, the presence of 10(-6) M Cu suppressed enzyme activities in the tissues examined, with a few exceptions such as AcP in ovaries and gut, AlP in liver, gills, gut, and testes, and LDH in liver. Hyperglycemia, hyperlactemia, hyperproteinemia, elevated blood free fatty acid (FFA) levels, and hypocholesterolemia were manifested in the fish exposed to 190 micrograms CuSO4/liter (1/3 96-hr TLm). Effects on the tissues included glycogenolysis (liver and skeletal muscles), glycogenesis (brain and heart), a marked rise in hepatic proteins, accumulation of FFAs in liver and skeletal muscles, and reduction in hepatic and gonadal cholesterol contents. After 8 weeks, a trend toward recovery was noted in the biochemical variables (except blood and hepatic protein levels).
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PMID:Short- and long-term effects of copper on the rosy barb (Puntius conchonius Ham.). 137 34

1. Enzyme modulation by cadmium in selected organs of the fish, Barbus conchonius (rosy barb), was investigated in vivo (48 hr exposure to 12.6 mg/l cadmium chloride) and in vitro (10(-6) M cadmium chloride). 2. The acetylcholinesterase (AchE) activity was depressed in the gills but stimulated in the skeletal muscles and brain in vivo. The hepatic, branchial, and renal acid phosphatase (AcP) activity decreased marginally in vivo but it was significantly increased in the gut and ovary. In vitro, except for the liver, the AcP activity was depressed in the selected organs. Collaterally, gut alkaline phosphatase (AlP) was significantly inhibited but a pronounced stimulation was noted in the kidneys and ovary in vivo. In vitro, the AlP activity was conspicuously elevated in the kidneys and gut, and moderately in the gills. 3. Cadmium inhibited the glutamate-oxaloacetate and glutamate-pyruvate transaminases (GOT and GPT) in the liver, gills and kidneys in vivo. In vitro, the GOT and GPT activities were decreased in the liver, gills and kidneys. The lactic dehydrogenase (LDH) was significantly stimulated by Cd in the heart in vivo but in vitro the metal inhibited the enzyme in the gills. 4. Enzymes in the liver, followed by those in the kidneys and gills seem to be most seriously affected by Cd poisoning in this fish.
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PMID:In vivo and in vitro effects of cadmium on selected enzymes in different organs of the fish Barbus conchonius Ham. (rosy barb). 168 47

1. Rosy barb (Puntius conchonius) were exposed to 181 micrograms/l mercuric chloride for 48 h and the activity of acid and alkaline phosphatases (AcP and AIP), aspartate aminotransferase (AAT), alanine aminotransferase (AIAT), lactic dehydrogenase (LDH), and acetylcholinesterase (AchE) were measured in vivo in several organs. 2. The AcP activity was inhibited in the liver, gills, kidneys, and gut but stimulated in the gonads. With the exception of kidney, the AIP activity showed an increase in all the organs examined. The AAT and AIAT were generally inhibited in different organs. An increase in LDH activity occurred in the cardiac and skeletal muscles while the AchE activity was considerably lowered in the brain, gills, and liver. 3. In vitro exposure to mercury at concentrations ranging between 10(-10) and 10(-4) M, inhibited the AIP, AAT, AIAT, LDH, and AchE activities in the tissues examined. The AcP activity was also depressed in all the tissues except in the testes, in which a marginal increase was noted. 4. The in vivo and in vitro effects of Hg were not of similar quality implying sequestration of toxic cations in the intact animals.
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PMID:Use of the fish enzyme system in monitoring water quality: effects of mercury on tissue enzymes. 198 72

Growth, feed conversion, serum chemistry and gross slaughter characteristics were determined in 20 steers (initially 9 mo of age, 231 +/- 18 kg) receiving daily injections of either saline (S) or recombinantly derived bovine somatotropin (rBST, 20.6 mg/d) for 112 d. Live weight gains were 15% greater for steers treated with rBST than for those treated with S. Feed intake was not different between S- and rBST-treated steers; thus, feed conversion was 12% more efficient in rBST steers. Scanogram backfat measurements were not affected by treatments. Serum electrolytes, protein, glucose and most enzyme activities were similar in S and rBST steers. Serum urea, creatinine and cholesterol (toward the end of treatment) concentrations, however, were lower (P less than .05) in rBST steers, suggesting that nitrogen retention was increased and lipid turnover was decreased by rBST. Total (P less than .1) and conjugated (P less than .05) bilirubin concentrations and glutamate-pyruvate transaminase activity (P less than .05) were lower in rBST steers. Carcass weights were not altered, but dressing percentages were lower (P less than .05) in rBST steers. This indicated that weight gain response to rBST was primarily in noncarcass components; further examination showed that this gain was predominantly in gut fill (approximately 2/3 of the greater live weight gain in rBST steers). Alternative protocols, such as administering the hormone to younger animals and (or) for a longer duration, may be necessary in order to achieve desirable responses in carcass growth.
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PMID:Growth and metabolism in somatotropin-treated steers: I. Growth, serum chemistry and carcass weights. 228 55

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.
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PMID:Copper protects against galactosamine-induced hepatitis. 365 8

The urinary metabolic excretion profile of acetaminophen (A) was reexamined in adult male Sprague-Dawley rats after administration of a single intraperitoneal (i.p.) or per oral (p.o.) dose of 100 or 750 mg/kg to 4 groups of animals, followed by collecting urines at 8, 24, 48 and 72 hr. The higher dose was administered in the form of a micronized suspension. The amounts of glucuronide, sulfate and mercapturate of A and unchanged A excreted in the urines were measured as a function of time. The pattern of urinary metabolic excretion of A was found to be dependent not only on the dose, but also on its route of administration as well as on the time of urine collection. When A was administered orally, the drug appears to be subjected to a gut and/or gut-wall first-pass elimination. The mean total urinary recovery of the drug was 70% after 72 hr following the administration of the higher dose of A. The hepatorenal toxicity was assessed by measuring the levels of serum glutamic-pyruvic transaminase activity and of urinary creatinine. The higher dose of A showed the potential to produce hepatic and renal toxicity when given i.p., but not when given orally. These toxic effects seem to be related with a high percentage of urinary A mercapturate and unchanged A when A was given i.p. as compared to those when it was given orally.
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PMID:Effects of route of administration on the dose-dependent metabolism of acetaminophen in rats: relationship with its toxicity. 375

A specific radioimmunoassay (RIA) has been developed that has sufficient sensitivity to allow measurement of the changes in plasma and tissue glutathione S-transferase (GST) YaYa concentrations which occur following thyroid hormone administration in the rat. Using the RIA it was demonstrated that the only tissues that had significant amounts of GST YaYa were liver, small gut and kidney. Administration of triiodothyronine (T3) or thyroxine (T4) resulted in increases in plasma GST YaYa concentration and in animals given high doses of T4 plasma alanine aminotransferase activity was also elevated. Thyroid hormone administration produced a significant fall in the hepatic content of GST YaYa and in total GST activity, as assessed using 1-chloro-2,4-dinitrobenzene as substrate. It is concluded that the elevated plasma GST YaYa concentrations observed following administration of thyroid hormones result from hepatic damage, not from induction of hepatic synthesis of the enzyme.
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PMID:Hepatic damage in the rat following administration of thyroxine or triiodothyronine, assessed by measurement of plasma glutathione S-transferase YaYa concentrations. 381 55

Circulating immune complexes (CIC) were measured in 133 biopsy-proven patients with various liver diseases. The correlation between CIC levels and other laboratory findings was investigated in each disease group, in order to assess if the increased C1q-binding activity found in these patients was related to particular features of the disease. CIC levels were not significantly different in HBsAg-positive and HBsAg-negative patients. No correlation was found between CIC levels and serum bilirubin, AST, ALT and C3 levels. A negative correlation with C4 levels and a positive correlation with immunoglobulin levels were found in the majority of the patients, while prothrombin time and albumin levels were negatively correlated to CIC levels only in patients with chronic active hepatitis. Increased CIC levels could represent a response to gut-associated antigens, a passive accumulation due to reduced hepatic function or both.
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PMID:Significance of circulating C1q-binding activity in chronic liver disease: a study of 133 cases. 633 89

We report that keratin 8 (mK8) gene disruption causes colorectal hyperplasia in FVB/N mice. The intestinal lesions affect uniformly the cecum, colon, and rectum but not the small intestine. The elongation of the crypts is accompanied by an inflammation of the lamina propria and submucosa. Hepatic, renal, and pancreatic functions tested in clinical assays are within nonpathological range, suggesting that the major defect lies in colonic epithelial cells. Still, small but consistent elevation in the hepatic enzymes alanine (AST) and asparate (ALT) aminotransferase are observed, along with a 70% increase in spleen weight. No homozygous mouse line has been established, because of a markedly reduced fertility of the mK8-/- females. Previously, we reported that the mK8- targeted mutation causes embryonic lethality in (C57B1/6x129Sv) mice. This strong effect of the genetic background on the mK8- mutant phenotype emphasizes the importance of using several inbred mouse strains to reveal the polygenic contribution to mutant phenotypes. Our results demonstrate that genetic modifiers of K8/K18 filament functions, with profound effects on embryogenesis and gut functional integrity, are differentially active in the FVB/N and C57B1/6 genetic backgrounds. More importantly, the increase in mK8-/- gut epithelial cell number, rather than cell disruption, contrasts with the known function of epidermal keratins in providing mechanical strength.
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PMID:Colorectal hyperplasia and inflammation in keratin 8-deficient FVB/N mice. 752 56


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