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At least 487 records · Page 27Linked to original sources
PubMed1982

Exercise in rats with liver injury induced by carbon tetrachloride or bile duct obstruction. Blood cholic acid and liver histology.

UNLABELLED: Tolerance of exercise in rats with liver injury was evaluated by the response of plasma cholylglycine (CG) and by liver histology in two experiments with CCl4 hepatocellular damage and in two other experiments with cholestatic liver injury induced by obstruction of the common bile duct. (1) Rats swimming daily for 1 h while exposed to five successive doses of CCl4 and studied at rest, had a trend (P less than 0.06) to higher CG and a higher plasma SGPT (P less than 0.05) than sedentary CCl4 rats. (2) In rats recovering from four successive doses of CCl4 there were no differences between CG curves before, during, and after exercise, except at 48 h of recovery when exercise elevated CG (P less than 0.05). (3) Sixteen days after ligation of the bile duct CG was high but not affected by exercise, 45 days after ligation exercise resulted in further increase of CG (P less than 0.05). (4) When ligation of the bile duct lasted only 24 h, exercise prior to release of the obstruction did not affect CG. Exercise 8 h and 27 h after release of ligation resulted in an increase in CG (P less than 0.05). Return to pre-exercise CG occurred 30 min after exercise. CONCLUSION: CG was a useful indicator of liver injury showing a positive correlation with the CCl4 dose and a negative correlation with recovery from CCl4. Exercise had only mildly adverse effect in hepatotoxic and cholestatic liver injury. CG appeared to respond more sensitively to exercise after release of bile duct obstruction than in CCl4 hepatocellular injury.

Alanine Transaminase↗
PubMed1976

Side chain hydroxylations in biosynthesis of cholic acid. 25- and 26-Hydroxylation of 5beta-cholestane-3alpha, 7alpha, 12alpha-triol by reconstituted systems from rat liver microsomes.

25- and 26-Hydroxylation of 5beta-cholestane-3alpha, 7alpha, 12alpha-triol was studied with reconstituted systems from rat liver microsomes consisting of partially purified cytochrome P -450, NADPH-cytochrome P -450 reductase, a phospholipid, and an NADPH -generating system. Cytochrome P -450 was prepared either by sodium cholate treatment and ammonium sulfate fractionation or by subtilisin and sodium deoxycholate treatment followed by DEAE-cellulose chromatography. No side chain hydroxylation was observed when cytochrome P-450 was omitted. With ammonium sulfate-fractionated cytochrome P-450 25- and 26-hydroxylation was stimulated 5- to 8-fold by addition of NADPH-cytochrome P-450 reductase. With subtilisin-treated cytochrome P-450 an almost absolute requirement for NADPH-cytochrome P-450 reductase was observed. Omission of lipid did not reduce the rate of hydroxylation. Centrifugation of the cytochrome P-450 preparation at 100,000 X g for 1 hour just before incubation increased markedly lipid dependency. A significant difference between 25- and 26-hydroxylation was observed with respect to substrate saturation. The stimulatory effect of phenobarbital treatment on 25-hydroxylation and the inhibitory effect of this treatment on 26-hydroxylation were associated with the cytochrome P-450 fraction. The use of increasing amounts of sodium cholate in the solubilization of cytochrome P -450 resulted in a gradual decrease of 25-hydroxylase activity and a gradual increase of 26-hydroxylase activity. 25- and 26-Hydroxylase activities were separated partially by chromatography of subtilisintreated cytochrome P-450 fraction on DEAE-cellulose. The question whether different species of cytochrome P-450 are involved in 25- and 26-hydroxylation is discussed.

Animals↗
PubMed1984

Transformation of 4-cholesten-3-one and 7 alpha-hydroxy-4-cholesten-3-one into cholestanol and bile acids in cerebrotendinous xanthomatosis.

In order to determine whether cholestanol and bile acids are derived from the same precursor, key intermediates of both biosynthetic pathways beyond cholesterol were administered intravenously to a patient with cerebrotendinous xanthomatosis and to a control subject. After pulse-labeling with [4-14C]4-cholesten-3-one and [G-3H]7 alpha-hydroxy-4-cholesten-3-one, cholestanol, cholesterol, and the two primary bile acids, cholic acid and chenodeoxycholic acid were isolated from specimens of bile. Each compound was purified by thin-layer chromatography and conclusively identified by gas-liquid chromatography-mass spectrometry. In other studies, the in vitro formation of 4-cholesten-3-one from cholesterol was measured in hepatic microsomal fractions prepared from a subject with cerebrotendinous xanthomatosis and from 3 control individuals. In all subjects, cholic acid and chenodeoxycholic acid were labeled with tritium, but neither cholesterol nor cholestanol contained this isotope. In contrast, 14C was detected in the cholestanol fraction with trace amounts in chenodeoxycholic acid, cholic acid, and cholesterol. Hepatic microsomes prepared from liver biopsy specimens obtained from a subject with cerebrotendinous xanthomatosis produced three times more 4-cholesten-3-one than the controls. The results indicate that 4-cholesten-3-one was converted primarily into cholestanol and 7 alpha-hydroxy-4-cholesten-3-one into cholic acid and chenodeoxycholic acid. Neither ketonic steroid was transformed into cholesterol. The increased production of cholestanol in cerebrotendinous xanthomatosis may be accounted for by enhanced hepatic formation of 4-cholesten-3-one. 7 alpha-Hydroxy-4-cholesten-3-one is a precursor of bile acids, but not of cholestanol.

Adult↗
PubMed1999

Bile salt deconjugation by lactobacillus plantarum 80 and its implication for bacterial toxicity

The effects of bile salts on the survival of lactobacilli were investigated using glycocholic acid, cholic acid and deoxycholic acid as model compounds and the bile salt hydrolase active Lactobacillus plantarum 80 (BSH+) and its BSH negative mutant. The detrimental effects of cholic acid, i.e. growth inhibition and cytotoxicity at a concentration of 1 and 5 mmol l-1, respectively, were considered to be due to the hydrophobic protonated form of the molecule, which brings about membrane damage. The conversion of glycocholic acid to cholic acid by the BSH active L. plantarum 80 caused a growth inhibition which was comparable with the inhibition observed in the broth supplemented with 1 mmol l-1 cholic acid. Deoxycholic acid caused toxicity through membrane damage when the compound was in solution. Its toxicity disappeared in the culture broth as the molecule precipitated. In case of cholic acid, the toxicity could be removed by buffering the solution at pH 7.0. It was calculated that at this pH most of the cholic acid molecules were ionized. The results led to the formulation of an extended hypothesis about the ecological significance of bile salt transformations. Primary deconjugation is carried out to counteract intracellular acidification. Yet, the deconjugated molecule can be harmful at moderately acidic pH-values. In this case, the BSH+ strains could effectively profit from their activity in case they are associated with 7alpha-dehydroxylating bacteria which dehydroxylate the deconjugated bile salts. The dehydroxylated molecule has a low solubility and precipitates at moderately acidic pH.

Journal Article↗
PubMed1984

Radioimmunoassay of serum conjugated cholic acid in hepatic murine schistosomiasis.

Cholylglycine levels were measured by radioimmunoassay in sera from 10 control CFI female mice and 22 CFI female mice experimentally infected with Schistosoma mansoni. Cholylglycine was significantly elevated in sera of all but one of the chronically infected animals. Serum aspartate transaminase was within normal limits in all the infected animals; while five infected mice had elevated serum alkaline phosphatase and all these five also had high levels of serum cholylglycine. Marked hepatic histopathological changes were demonstrated in all the infected animals. The data suggest that serum cholylglycine is a highly sensitive index for hepatic dysfunction in chronic hepatic schistosomiasis mansoni.

Alkaline Phosphatase↗