Biomedical subjects

G Parmentier

Publications and source records attributed to G Parmentier.

At least 37 records · Page 2Linked to original sources

PubMed1989

By-products in the analysis of beta-muricholic acid in biological samples as methyl ester triacetate.

By-products were formed on analysis of beta-muricholic acid (3 alpha, 6 beta, 7 beta-trihydroxy-5 beta-cholan-24-oic acid) in biological samples by a method involving acid-catalyzed solvolysis of sulfate esters in acetone-methanol, followed by perchloric acid-catalyzed acetylation with acetic anhydride-acetic acid. These products have been identified by mass spectrometry and nuclear magnetic resonance as methyl 3-0,6-0-diacetyl-7-0-(1-methyl-3-oxo-1-butenyl)- and methyl 3-0,7-0-diacetyl-6-0-(1-methyl-3-oxo-1-butenyl)-beta-muricholate, methyl 3-0, 6-0-diacetyl- and methyl 3-0, 7-0-diacetyl-beta-muricholate, and a methyl diacetoxy-cholen-24-oate.

Acetylation↗

PubMed1989

Activation and peroxisomal beta-oxidation of fatty acids and bile acid intermediates in liver from Bombina orientalis and from the rat.

1. Bombina orientalis excretes mainly C27 bile acids: trihydroxycoprostanic and varanic acids. More than 90% of the trihydroxycoprostanic acid (THCA) present in the bile, was conjugated with taurine; varanic acid was present in the unconjugated form. 2. Trihydroxycoprostanoyl-CoA (THC-CoA) synthetase activity, required for the formation of the taurine conjugate, was present in the liver of Bombina orientalis. 3. Peroxisomal beta-oxidation, which catalyzes the oxidation of fatty acids as well as the conversion of C27 bile acids into C24 bile acids in rat and human liver, could be detected in liver of Bombina orientalis when palmitoyl-CoA was used as substrate, but not when trihydroxycoprostanoyl-CoA (THC-CoA) was used.

Animals↗

PubMed1989

Selective activity of several cholic acid derivatives against human immunodeficiency virus replication in vitro.

Several cholic acid derivatives such as taurolithocholic acid, lithocholic acid 3-sulfate, taurolithocholic acid 3-sulfate, and glycolithocholic acid 3-sulfate were shown to inhibit selectively the replication of human immunodeficiency virus type 1 (HIV-1) in vitro. These compounds completely protected MT-4 cells against HIV-1-induced cytopathogenicity at a concentration of 100 micrograms/ml, whereas no toxicity for the host cells was observed at 200 micrograms/ml. They also inhibited HIV-1 antigen expression in HIV-1-infected CEM cells. The bile acids (cholic acid, deoxycholic acid, chenodeoxycholic acid, and lithocholic acid) did not show any inhibitory effect on HIV-1 replication at concentrations that were not toxic to the host (MT-4) cells. From a structure-function analysis of a number of cholic acid derivatives, the presence of either a sulfonate (as in the tauro conjugates) or a sulfate group as well as the "litho" configuration appeared to be necessary for the expression of anti-HIV-1 activity. The active cholic acid derivatives did not directly inactivate the virus particles at the concentrations that were not toxic to the host cells. Lithocholic acid 3-sulfate, taurolithocholic acid 3-sulfate, and glycolithocholic acid 3-sulfate, but not taurolithocholic acid, partially inhibited virus adsorption to MT-4 cells. These three compounds were also inhibitory to the reverse transcriptase activity associated with HIV-1.

Adsorption↗

PubMed1988

Beta-oxidation of the carboxyl side chain of prostaglandin E2 in rat liver peroxisomes and mitochondria.

Rat liver and kidney homogenates, fortified with the appropriate cofactors, produced H2O2 when incubated with prostaglandin (PG) E2 or its CoA ester (PGE2-CoA), indicating that PGE2-CoA served as substrate for acyl-CoA oxidase, the first enzyme of peroxisomal beta-oxidation. PGE2-CoA oxidase was stimulated to the same extent as palmitoyl-CoA oxidase by treatment of rats with the peroxisome proliferator clofibrate. Subcellular fractionation confirmed that both oxidase activities were located in peroxisomes. When highly purified peroxisomes were incubated with [1-14C]PGE2, radioactive oxidation products were released, demonstrating that peroxisomes were capable of catalyzing the complete beta-oxidation sequence. However, PGE2 beta-oxidizing activity was expressed only when isolated microsomes were added to the purified peroxisomes, indicating that PGE2-CoA synthetase is located in the endoplasmic reticulum. Cofactor requirements for peroxisomal [1-14C]PGE2 and [1-14C]palmitate oxidation were identical, and oxidation was not inhibited by cyanide. [1-14C]PGE2 was also beta-oxidized by highly purified mitochondrial fractions, devoid of peroxisomes, when microsomes were added. Mitochondrial [1-14C]PGE2 and [1-14C]palmitate oxidation was CoA- and ATP-dependent and inhibited by cyanide. Palmitate oxidation was carnitine-dependent, but PGE2 oxidation was not. Acyl-CoA dehydrogenase activity, but not carnitine acyltransferase activity, was detected with PGE2-CoA as substrate. [1-14C]PGE2 oxidation in whole liver homogenates was only slightly inhibited by cyanide, indicating that peroxisomes oxidized the major portion of PGE2. The concentrations of PGE2 employed in these experiments exceeded the in vivo concentrations by several orders of magnitude. Therefore, we suggest that the urinary PG metabolite excretion be measured in patients with hereditary diseases in which peroxisomal or mitochondrial beta-oxidation is not functioning in order to clarify the role of each organelle in PG oxidation in vivo.

Animals↗

PubMed1988

[Budd-Chiari syndrome with thrombosis of the inferior vena cava. Treatment by mesenterico-innominate shunt].

We report two cases of patients, 12 and 28 years old, suffering from a Budd-Chiari syndrome with a thrombosed inferior vena cava, who were treated by a shunt interposed between the superior mesenteric vein and the left innominate vein. The aim of this shunt was to avoid pericardiotomy in these patients with peroperative ascites, in order to reduce the risk of pericarditis after surgery. A reinforced polytetrafluoroethylene prosthesis (Gore-Tex) was used, associated with an interposition jugular vein graft in the 12-year old child, alone in the other case. The left innominate vein was isolated through a midline sternotomy, and the prosthesis was placed in a retrosternal position. Operation and postoperative course were uneventful. All signs of ascites disappeared. The patients were free of symptoms, 8 and 4 months after surgery respectively. Shunt patency was documented by angiography and magnetic nuclear resonance.

Adult↗

PubMed1987

Inhibition of peroxisomal fatty acyl-CoA oxidase by antimycin A.

Peroxisomal fatty acyl-CoA oxidase was inhibited by micromolar concentrations of antimycin A, an inhibitor of mitochondrial respiration. The inhibition was observed with all three substrates tested, i.e. palmitoyl-CoA, trihydroxycoprostanoyl-CoA and hexadecanedioyl-CoA. The peroxisomal D-amino acid oxidase was also inhibited by antimycin, but the peroxisomal L-alpha-hydroxyacid oxidase and uric acid oxidase and the mitochondrial monoamine oxidase were not. The degree of inhibition of acyl-CoA oxidase by antimycin was strongly dependent on the amount of cellular protein present in the assay mixture: at a fixed antimycin concentration, the inhibition was gradually lost with increasing protein concentrations. At a fixed cellular protein concentration in the assay mixtures, the mitochondrial oxidation of glutamate or palmitoylcarnitine was inhibited at antimycin concentrations that were much lower than those required for the inhibition of fatty acyl-CoA oxidase. Our results, nevertheless, demonstrate that antimycin A must be used with caution, when it is added to homogenates or subcellular fractions in order to distinguish between mitochondrial and peroxisomal fatty acid oxidation.

Acyl-CoA Oxidase↗

PubMed1987

Influence of an estrone-desulfating intestinal flora on the enterohepatic circulation of estrone-sulfate in rats.

The fecal and urinary excretion of orally administered [4-14C]estrone-3-sulfate was studied in germfree (GF) rats, conventional (CV) rats and gnotobiotic rats selectively associated with estrone-desulfating and/or cecal-volume reducing microorganisms. The time required to excrete 50% of the total label recovered (t 1/2) was 22 h in CV rats vs 32 h in GF rats. Gnotobiotic rats selectively associated with a cecal volume-reducing flora (CRF rats) excreted the label even faster (t 1/2 = 13 h) than CV rats. Association of GF rats as well as CRF rats with estrone-desulfating microorganisms (termed S1 + S2 + R9 rats and CRF + S1 + S2 + R9 rats, respectively) led to a slower excretion of labeled products (t 1/2 = 38 h in S1 + S2 + R9 rats and t 1/2 = 27 h in CFR + S1 + S2 + R9 rats). Intestinal microbial desulfation also increased the relative part of the urinary excretion from 4% in GF rats to 8% in S1 + S2 + R9 rats and from 3% in CRF rats to 9% in CFR + S1 + S2 + R9 rats. We conclude that intestinal microbial desulfation enhances the enterohepatic circulation of orally administered estrone-3-sulfate.

Animals↗

PubMed1986

[Peridural anesthesia with procaine and fentanyl in a parturient with acute intermittent porphyria].

Acute intermittent porphyria is one of three severe hepatic porphyrias. Clinical manifestations include intermittent acute attacks of abdominal pain and neuropathy with an occasionally outcome. These attacks are often precipitated by endogenous (menstrual cycle and pregnancy in women) or exogenous factors (porphyrinogenic drugs). An epidural analgesia was performed during the labour of a pregnant woman with acute intermittent porphyria just after an acute attack of abdominal pain. Analgesia was obtained using procaine and fentanyl. The choice of drugs was based on available clinical reports and experimental studies of the porphyrinogenicity of drugs in animal models (rat in vivo and chick embryo in ovo).

Acute Disease↗

PubMed1986

Isolation of a rat intestinal Clostridium strain producing 5 alpha- and 5 beta-bile salt 3 alpha-sulfatase activity.

An unnamed sporeforming microorganism, termed Clostridium sp. strain S2, possessing bile salt sulfatase activity was isolated from rat intestinal microflora. The microorganism was a strictly anaerobic, nonmotile, gram-negative, asaccharolytic, sporeforming rod requiring CO2, vitamin K, and taurine; the guanine-plus-cytosine content of the DNA was 40.8 mol% (Tm), and the strain was tentatively classified as an atypical Clostridium species. Sulfatase activity was specific for 3 alpha-sulfate esters of 5 alpha- and 5 beta-bile salts, leaving the 3 beta-, 7 alpha-, and 12 alpha-sulfates unchanged. Strain S2 also deconjugated tauro- and glyco-conjugated bile salts and partially reduced into the corresponding 6 alpha-hydroxy bile salts. By these reactions, alpha-muricholate and beta-muricholate were more than 80% converted into hyocholate and omega-muricholate, respectively. In addition, strain S2 produced 12 alpha-hydroxysteroid dehydrogenase converting deoxycholate into 3 alpha-hydroxy-12-oxo-5 beta-cholanoate. When strain S2 was associated with gnotobiotic rats, the fecal bile salts were more than 90% desulfated and the fecal excretion of allochenodeoxycholate was five times lower than in control rats.

Animals↗

PubMed1986

Biotransformation of Unsaturated Long-Chain Fatty Acids by Eubacterium lentum.

Eubacterium lentum (33 strains) isomerized the 12-cis double bond of C(18) fatty acids with cis double bonds at C-9 and C-12 into an 11-trans double bond before reduction of the 9-cis double bond. The 14-cis double bond of homo-gamma-linolenic acid was isomerized by 29 strains into a 13-trans double bond. The same strains isomerized the 14-cis double bond of arachidonic acid into a 13-trans double bond and then isomerized the 8-cis double bond into a 7-trans double bond; the 13-cis double bond of 10-cis, 13-cis-nonadecadienoic acid was isomerized into a 12-trans double bond. None of these isomerization products was further reduced. Studies with resting cells showed optimal isomerization velocity at a linoleic acid concentration of 37.5 muM; higher concentrations were inhibitory. The pH optimum for isomerization was 7.5 to 8.5. The isomerase was inhibited by the sulfhydryl reagents iodoacetamide, bromoacetate, and N-ethylmaleimide and by the chelators EDTA and 1,10-phenanthroline.

Journal Article↗

PubMed1985

Influence of microbial bile salt desulfation upon the fecal excretion of bile salts in gnotobiotic rats.

The fecal excretion of intraperitoneally injected 24-14C-labeled taurocholate (TCA), taurolithocholate (TLCA) and the respective 3-sulfate esters (TCA-3-S; TLCA-3-S), were compared in germfree (GF) rats, conventional (CV) rats, and in gnotobiotic rats associated with Clostridium Cl-8 or this same strain Cl-8 plus the bile desulfating Clostridium S1, respectively. TCA and TLCA were about two times more rapidly excreted by CV animals than by GF animals; the time required for 50% excretion of total label injected (t 1/2) was 6.6 days vs 14.9 for TCA, and 4.4 vs 8.9 for TLCA. In GF and in CV animals, TCA-3-S and TLCA-3-S were excreted more rapidly than their nonsulfated analogues; the t 1/2 values of TCA-3-S and TCA were 2.7 days vs 14.9 in GF rats, and 3.1 vs 6.6 days in CV animals. The t 1/2 values of TLCA-3-S and TLCA were 2.7 days vs 8.9 in GF rats, and 1.5 vs 4.4 days in CV rats. In gnotobiotic rats associated with Clostridium strains S1 + Cl-8, fecal bile salts were nearly 100% deconjugated and desulfated and the 50% excretion times of TCA-3-S and TLCA-3-S approximated to those of TCA and TLCA in GF animals. T 1/2 of TCA-3-S in gnotobiotic S1 + Cl-8 animals was 12.2 days vs 14.9 for TCA in GF animals. In gnotobiotic S1 + Cl-8 animals the t 1/2 of TLCA and TLCA-3-S was 12.5 and 11.0 days, respectively. These results illustrate clearly the important effect the intestinal microflora has upon the metabolic half-life of bile salts. Moreover, they demonstrate that desulfation of bile salts by the intestinal microflora takes place in intestinal segments from where a certain degree of reabsorption is still possible, and thus point to the fact that microbial desulfation is an important variable in the overall elimination of bile salts.

Animals↗

PubMed1985

Bile acid abnormalities and the diagnosis of cerebro-hepato-renal syndrome (Zellweger syndrome).

The Zellweger or cerebro-hepato-renal syndrome (CHRS) is a congenital disorder characterized by cerebral dysfunction, craniofacial dysmorphic features, transient cholestasis and renal cysts. Patients fail to thrive, and usually die in their first year of life. In some cases, a definite diagnosis on purely clinical signs might not be possible. Several biochemical abnormalities have been observed in these patients and some of them have been tested as diagnostic markers. The aim of this study is to evaluate bile acid metabolites as biochemical markers of the CHRS. From a study of 20 CHRS patients, we conclude that screening for the presence of coprostanic acids and the C-29 dicarboxylic bile acid in serum or urine is for detection of CHRS and confirmation of the diagnosis.

Bile Acids and Salts↗

PubMed1984

Specificity of bile salt sulfatase activity in man, mouse and rat intestinal microflora.

Desulfation of bile acid 3-, 7- and 12-monosulfates was studied in incubates of fecal flora of man, rat and mouse. In anaerobic incubates, the 3 alpha-sulfates of the 5 beta-bile acids chenodeoxycholic acid and cholic acid, as well as the 3 alpha-sulfate of the 5 alpha-bile acid allochenodeoxycholic acid, were desulfated and further metabolized with the formation of a variety of metabolites. Desulfation yields were low in aerobically incubated samples, and aerobic subcultures were always negative. The 7- or 12-monosulfate esters of chenodeoxycholic acid and cholic acid were not hydrolyzed, neither anaerobically nor aerobically. High numbers (10(7) per 10(9) total count) of bile salt 3-sulfatase producing bacteria were present in rat cecal contents. No desulfating bacteria were detected in the proximal or medium small intestine of the rat, whereas low numbers were found in 2 out of 5 samples from the distal small intestine. These results reflect the predominantly anaerobic character of the bile salt sulfatase producing microflora in the intestine and suggest that the intestinal microflora of man, rat and mouse do not possess bile salt 7- or 12-sulfatase activity.

Anaerobiosis↗

PubMed1983

[The abdomen in multiple-injured patients. Comparative study on 225 multiple-injured patients with and without abdominal lesions. Incidence of abdominal complications].

Of 225 patients with multiple injuries and a high lesional score, 100 presented traumatic abdominal lesions. Comparison of the two groups confirmed both the usefulness and validity of a traumatic index and the reliability of abdominal puncture-lavage. Abdominal complications were analyzed. Mortality in all multiple injury cases, with or without abdominal lesions, was identical in this series where emergency surgery was performed only for lesions affecting vital organs, the mean age of patients with abdominal lesion being significantly lower. An attitude to adopt when deciding whether surgery is necessary is proposed.

Abdominal Injuries↗

PubMed1982

[Penetrating thoracic and abdominothoracic wounds. Results of treatment in 221 cases (author's transl)].

Overall mortality after treatment of 221 thoracic or abdominothoracic wounds was 5 p. cent in a recent series, mortality from bullet wounds being the double of that from other weapons. Isolated thoracic wounds without cardiac lesions have a good prognosis, whereas mortality after heart or abdominothoracic wounds remains high (12.5 p. and 14 p. cent respectively). Apart from those with severe hepatic injuries or wounds of the suprahepatic veins, most of the injured patients that died were in cardiac arrest on arrival. Different therapeutic attitudes are necessary for pure thoracic wounds and those involving the abdominothoracic region. It is essential to gain as much time as possible at all stages, particularly during transport of the injured and when deciding the course of treatment, to avoid losing patients with curable lesions.

Abdominal Injuries↗

PubMed1982

Structure of the side chain of the C29 dicarboxylic bile acid occurring in infants with coprostanic acidemia.

The structure of the side chain of the 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-C29 dicarboxylic bile acid occurring in body fluids of infants with coprostanic acidemia was investigated by means of mass spectrometry and nuclear magnetic resonance spectroscopy. The findings identified this bile acid as 3 alpha, 7 alpha, 12 alpha-trihydroxy-27a, 27b-dihomo-5 beta-cholestane-26,27b-dioic acid (3 alpha, 7 alpha, 12 alpha-trihydroxy-27-carboxymethyl-5 beta-cholestan-26-oic acid).

Cholestanols↗

PubMed1982

[Esophageal perforation during tracheal intubation. Report on 6 cases. (author's transl)].

Perforation of the esophagus and hypopharynx followed tracheal intubation for general anesthesia or during intensive care in 6 patients. Circumstances favorable to the production of these lesions, and diagnostic features enabling early diagnosis are discussed. Simple surgical procedures and intensive postoperative care resulted in recovery in 5 of the 6 cases.

Aged↗

PubMed1981

A further study of the bile acids in infants with coprostanic acidemia.

The structure of the bile acids in serum of infants with coprostanic acidemia was further investigated. The identity of 3 alpha-hydroxy-5 beta-cholestan-26-oic acid and 3 beta-hydroxy-5-cholesten-26-oic acid was confirmed. The biosynthesis of the 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-C29 dicarboxylic bile acid does not start from beta-sitosterol.

Acidosis↗