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Biomedical subjects

G Siest

Publications and source records attributed to G Siest.

At least 145 records · Page 8Linked to original sources

Glycosylation of gamma-glutamyltransferase is modified by ethanol in H5-6 hepatoma cell line.

The H5-6 cultured rat hepatoma cell line was used to investigate the post-translational maturation of gamma-glutamyltransferase (GGT) and the effects of acute ethanol administration on the expression and glycosylation of this membrane-bound glycoprotein. We found that the two subunits of H5-6 GGT with molecular masses of 55 and 33 kDa were derived from a single glycosylated precursor of 80 kDa. In addition, signals of high molecular mass (more than 90 kDa) were detected. In vitro deglycosylation experiments indicated that N-linked sugars represented about 25% of the molecular weight of the H5-6 enzyme. By use of serial lectin affinity technique, we showed that N-linked sugar chains were mainly of the biantennary complex and hybrid-type, without fucose linkage to the innermost N-acetyl-glucosamine. Ethanol treatment did not seem to affect the expression of GGT and the sialic acid content of the enzyme, but altered its oligosaccharide chain composition both quantitatively and qualitatively.

Animals↗

Drug metabolizing enzymes related to laboratory medicine: cytochromes P-450 and UDP-glucuronosyltransferases.

Many studies on drug metabolism have been carried out during the last decades using protein purification, molecular cloning techniques and analysis of polymorphisms at phenotype and genotype levels. These researchers led to a better understanding of the role of drug metabolizing enzymes in the biotransformation of drugs, pollutants or foreign compounds and of their use in laboratory medicine. The metabolic processes commonly involved in the biotransformation of xenobiotics have been classified into functionalization reaction (phase I reactions), which implicate lipophilic compounds. These molecules are modified via monooxygenation, dealkylation, reduction, aromatization, hydrolysis and can be substrates for the phase II reactions, often called conjugation reactions as they conjugate a functional group with a polar, endogenous compound. This review, devoted to cytochromes P-450 (CYP) and UDP-glucuronosyltransferases (UGT), describes essentially the genetic polymorphisms found in humans, their clinical consequences and the methods to assess the phenotypes or genotypes, with a view to studying the interindividual differences in drug monooxygenation and drug glucuronidation. Variations in drug glucuronidation reported here focused essentially on variations due to physiological factors, induction, drug interactions and genetic factors in disorders such as Gilbert's Syndrome and Crigler-Najjar type I and II diseases.

Cytochrome P-450 Enzyme System↗

Localization of drug-metabolizing enzyme activities to blood-brain interfaces and circumventricular organs.

The brain, with the exception of the choroid plexuses and circumventricular organs, is partially protected from the invasion of blood-borne chemicals by the specific morphological properties of the cerebral micro-vessels, namely, the tight junctions of the blood-brain barrier. Recently, several enzymes that are primarily involved in hepatic drug metabolism have been shown to exist in the brain, albeit at relatively low specific activities. In the present study, the hypothesis that these enzymes are located primarily at blood-brain interfaces, where they form an "enzymatic barrier," is tested. By using microdissection techniques or a gradient-centrifugation isolation procedure, the activities of seven drug-metabolizing enzymes in isolated microvessels, choroid plexuses, meningeal membranes, and tissue from three circumventricular organs (the neural lobe of the hypophysis, pineal gland, and median eminence) were assayed. With two exceptions, the activities of these enzymes were higher in the three circumventricular organs and cerebral microvessel than in the cortex. Very high membrane-bound epoxide hydrolase and UDP-glucuronosyltransferase activities (approaching those in liver) and somewhat high 7-benzoxyresorufin-O-dealkylase and NADPH-cytochrome P-450 reductase activities were determined in the choroid plexuses. The pia-arachnoid membranes, but not the dura matter, displayed drug-metabolizing enzyme activities, notably that of epoxide hydrolase. The drug-metabolizing enzymes located at these nonparenchymal sites may function to protect brain tissue from harmful compounds.

Animals↗

Effect of alcohol consumption on blood antioxidant nutrients and oxidative stress indicators.

The effects of alcohol consumption on plasma concentrations of antioxidant vitamins (alpha-tocopherol and ascorbic acid), selenium, and markers of oxidative stress, especially malondialdehyde (MDA) and autoantibodies directed to MDA adducts to proteins (Ig-NH2-MDA) were investigated in a large population of 417 supposedly healthy men who consumed only low or moderate amounts of alcohol as compared with 102 alcoholic patients without severe liver disease, who were studied both before and after 21 d of withdrawal treatment. Plasma concentrations of alpha-tocopherol, ascorbic acid, and selenium were lower in alcoholics than in men who drank low amounts of alcohol (P < or = 0.001), whereas MDA and Ig-NH2-MDA were higher (P < or = 0.001). Plasma concentrations of alpha-tocopherol and selenium remained unchanged after the withdrawal period, whereas ascorbic acid (P < or = 0.01), MDA, and Ig-NH2-MDA concentrations decreased (P < or = 0.001). Adjustment of data for circulating lipids and nutritional intake suggests a specific effect of alcohol on antioxidant vitamins, independent of nutritional status.

Adult↗

DNA polymorphisms of human apolipoprotein A-IV gene: frequency and effects on lipid, lipoprotein and apolipoprotein levels in a French population.

Genetic polymorphisms of apolipoprotein (apo) A-IV have been shown to influence lipoprotein metabolism in some human populations. In this study, we have evaluated the physiological effect of three apo A-IV polymorphisms (Gln360- > His, Thr347- > Ser and XbaI within the second intron of the apo A-IV gene), in a French population, on seven quantitative traits: total cholesterol and triglycerides, cholesterol of HDL, apo A-IV, apo B, apo A-I and glucose. The polymorphism at amino-acid 360 was determined by direct analysis of polymerase chain reaction products. The allele frequencies were 0.92 for the A-IV1 and 0.08 for the A-IV2 allele. The genetic polymorphism at codon 347 was investigated by allele-specific oligonucleotide hybridization. The allele frequencies of the two alleles, A-IV347Thr and A-IV347Ser, were 0.78 and 0.22, respectively. The XbaI polymorphism was investigated by polymerase chain reaction followed by XbaI restriction enzyme digestion of the amplified products. The frequencies of the two apo A-IV alleles, XbaI-1 and XbaI-2, were 0.79 and 0.21, respectively. None of the three apo A-IV polymorphisms had a significant effect on lipoprotein, apolipoprotein and glucose levels.

Adult↗

The relation of alcohol consumption to serum carotenoid and retinol levels. Effects of withdrawal.

The effects of alcohol consumption on plasma concentrations of retinol and various carotenoids (beta-carotene, alpha-carotene, zeaxanthin-lutein, lycopene and beta-cryptoxanthin) were studied in a control population of 118 supposedly healthy men consuming low or moderate amounts of alcohol, and 95 alcoholic patients without severe liver disease before and after a withdrawal treatment of 21 days. There was no significant difference between alcoholics and controls regarding plasma retinol level. Conversely, plasma concentrations of all the carotenoid fractions were significantly lower in the alcoholic group than in the low drinker group. After withdrawal, plasma levels of all the carotenoids increased whereas retinol concentration diminished. Adjustment of data for various potential confounding factors especially including nutritional intake suggests an effect of alcohol on plasma carotenoids and a specific effect of withdrawal on plasma retinol, both of them being not only related to nutritional status.

Adult↗

Stable expression of enzymatically active human pancreatic lipase in V79 cells: purification and characterization of the recombinant enzyme.

The serum activity of human pancreatic lipase (HPL; EC 3.1.1.3), the main lipolytic enzyme secreted by the pancreas, is a valuable marker of pancreatic disorders. However, determining lipase activity in human serum is difficult because the substrates used vary in their lipase specificity. A lipase reference material is therefore needed. We describe the production of recombinant HPL (rHPL) in V79 Chinese hamster lung cells. A cDNA encoding the sequence of HPL was subcloned into the pcDNAI eukaryotic expression vector, which was then used to transfect V79 cells. The 50-kDa purified recombinant enzyme is fully active, is glycosylated, and has a pI of 7.0. The catalytic properties of rHPL, determined by using triolein as the substrate, were similar to those of the native enzyme. The V79rHPL cell line we developed might be useful for the production of rHPL suitable for the preparation of a reference material.

Animals↗

A recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UDP-glucuronosyltransferase 2B1) stably expressed in V79 cells catalyzes the glucuronidation of morphine, phenols, and carboxylic acids.

V79 (Chinese hamster lung fibroblast) cell lines expressing a functional recombinant phenobarbital-inducible rat liver UDP-glucuronosyltransferase (UGT), i.e., UGT2B1, were established. Western blot analysis of positive colonies, using anti-rat liver UGT antibodies, revealed the presence of an immunoreactive polypeptide of the expected molecular mass of 52 kDa. The substrate specificity of the recombinant enzyme toward > 100 compounds was determined. Phenolic and alcoholic substrates included 4-methylumbelliferone, 4-hydroxybiphenyl, chloramphenicol, and testosterone, but a range of carboxylic acids of both endogenous (medium-chain saturated fatty acids, long-chain polyunsaturated fatty acids, and bile acids) and exogenous (profen nonsteroidal anti-inflammatory drugs, fibrate hypolipidemic agents, and sodium valproate) origin were also accepted, indicating that the enzyme was capable of forming both ether- and ester-type glucuronides from various structurally unrelated compounds. Determination of apparent kinetic constants for the glucuronidation by UGT2B1 of selected aglycones revealed a high maximal velocity toward the 3-position of morphine (49.3 +/- 2.2 nmol/min/mg of protein), compared with other known substrates such as 4-methylumbelliferone (2.67 +/- 0.11 nmol/min/mg of protein) or clofibric acid (0.06 +/- 0.02 nmol/min/mg of protein). To gain a better insight into the mechanisms underlying the apparently wide substrate specificity of UGT2B1, series of structurally related compounds were tested as potential substrates. The rate of glucuronidation of unbranched saturated fatty acids and omega,omega,omega-triphenylalkanoic acids increased progressively with increasing alkyl chain length and then declined, with the best substrates in these two homologous series being decanoic acid and 4,4,4-triphenylbutanoic acid, respectively. Glucuronidation of para-substituted phenols always proceeded at a higher rate than that of the corresponding para-substituted benzoic acids. This could mean that the aglycon hydroxyl group was better positioned in the enzyme active site in the case of phenols. Alternatively, if the initial interaction with the enzyme required the aglycon to be in the protonated uncharged form, then the observation could be explained by the difference in ionization between phenols and benzoic acids at the incubation pH used. The introduction of a bulky alkyl group into the para-position led to increases of up to 300-fold in the rate of glucuronidation, probably as a result of the increased aglycon lipophilicity. Finally, the enzyme showed a degree of stereo- and regiospecificity, preferring (S)-ibuprofen to the R-enantiomer (Vmax/Km, 3.06 and 1.10 microliters/min/mg of protein, respectively) and glucuronidating lithocholic acid but not hyodeoxycholic acid, which differs by only a single hydroxyl group.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Determination of the human liver UDP-glucuronosyltransferase 2B4 domains involved in the binding of UDP-glucuronic acid using photoaffinity labeling of fusion proteins.

The interactions between UDP-glucuronic acid and two human liver UDP-glucuronosyltransferase 2B4 peptides (14-150 and 299-446) purified from E. coli as Staphylococcus aureus protein A fusion proteins have been investigated. Photoaffinity labeling with azidonucleotides ([beta-32P]5N3UDP-Glucuronic acid and [beta-32P]5N3UDP-Glucose) and competition experiments with UDP-glucuronic acid and structurally related compounds emphasized the presence of a specific UDP binding site between amino acids 299 and 446. Moreover, competition experiments strongly suggested an interaction between the amino terminal part of the protein and glucuronic acid. It would involve an electrostatic bond in the binding of the cosubstrate via the carboxyl group of UDP-glucuronic acid and a positively charged amino acid of the N-terminal domain of the enzyme.

Affinity Labels↗

Glucuronidation of hyodeoxycholic acid in human liver. Evidence for a selective role of UDP-glucuronosyltransferase 2B4.

Monospecific polyclonal antibodies were raised against a variable amino-terminal domain (amino acids 14-150) of a human liver form of UDP-glucuronosyl-transferase conjugating bile acids, UGT2B4 (Jackson, M. R., McCarthy, L. R., Harding, D., Wilson, S., Coughtrie, M. W., and Burchell, B. (1987) Biochem. J. 242, 581-588), expressed as a fusion protein in Escherichia coli. The antibodies were able to recognize the protein, stably expressed in a genetically engineered eukaryotic V79 cell line, against which they were directed. The specificity of these antibodies allowed their use for analyzing the substrate specificity of this isoform in human liver, as well as for determining its contribution to the total hepatic and extra-hepatic glucuronidation of hyodeoxycholic acid. Western blot analysis of microsomal proteins demonstrated the presence of UGT2B4 exclusively in human liver and not in human kidney. In human liver microsomes, the antibodies were able to inhibit and precipitate up to 90% of the total hyodeoxycholic acid 6-O-glucuronidation activity, but had no effect on activities toward several other substrates, such as phenols, bilirubin, or other bile acids, especially hyocholic acid and the steroids 4-hydroxyesterone and estriol. Moreover, Western blot analysis and immunoinhibition studies of human liver microsomes from healthy patients and from patients presenting liver diseases revealed a good correlation between the glucuronidation rate of hyodeoxycholic acid and the UGT2B4 expression level. The absence of immunoinhibition of hyodeoxycholic acid conjugation with UDP sugars other than UDP-glucuronic acid suggests the involvement of different enzymatic systems in the glucosidation and xylosylation of hyodeoxycholic acid. Altogether, the results provided strong evidence for the specific and predominant involvement of UGT2B4 in the 6-O-glucuronidation of this bile acid via a UDP-glucuronic acid-dependent mechanism.

Animals↗

Purification and characterization of a catalytically active human liver UDP-glucuronosyltransferase expressed as a fusion protein in E. coli.

The purification and the characterization of functional human liver UDP-glucuronosyltransferase 2B4 produced as a Staphylococcus aureus protein A fusion protein in E. coli are described. The purified fusion protein was able to catalyze the glucuronidation of hyodeoxycholic acid, the major substrate described for this isoform to date. The effects of the amount and the nature of the phospholipids upon reconstitution into phospholipid micelles were investigated. Apparent determined Km values for hyodeoxycholic acid and UDP-glucuronic acid were 0.55 and 0.43 mM, respectively. Moreover, photoaffinity labelling of the fusion protein with a photoactivatable analog of UDP-glucuronic acid strongly suggested that this recombinant protein exhibited similar binding properties as the microsomal protein, which emphasizes its use for further structural analyses.

Affinity Labels↗

The 5' untranslated region of the human gamma-glutamyl transferase mRNA contains a tissue-specific active translational enhancer.

We report the functional and structural analysis of the 5' untranslated region (5'UTR) of human hepatoma HepG2 gamma-glutamyltransferase (GGT) mRNA. Transient expression of a hybrid GGT-luciferase gene in HepG2, MIA-Pa-Ca-2 and MG 63 cell lines shows that this 5'UTR acts as a tissue-specific translational enhancer. Evidence for transcripts with multiple 5'UTR coding for HepG2 GGT was obtained by RNase protection. Computer analysis of this 5'UTR detected the existence of a stable stem and loop structure containing multiple steroid modulatory elements.

Base Sequence↗

Establishment of a V79 transfected cell line highly producing recombinant human gamma-glutamyltransferase.

gamma-Glutamyltransferase (GGT) is a glutathione-metabolizing enzyme whose activity variations in serum and organs are valuable markers of preneoplastic processes, alcohol abuse and induction by drugs. To elucidate the implication of GGT in various metabolic pathways, we established a stable transfected V79 cell line highly producing the human GGT. A full length cDNA, encoding the human hepatoma Hep G2 GGT, was subcloned into an expression vector under the control of the SV40 early promoter and was used to transfect V79 cells. A cell line was selected, exhibiting a GGT activity of 2 units per mg of protein, one of the highest levels reported to date. The recombinant GGT purified from this cell line showed the expected heterodimeric structure, with two subunits existing as sialylated and differentially glycosylated isoforms, with mean molecular masses of 80 and 29 kDa. Catalytic features were found to be identical to those of human serum and Hep G2 GGTs. Thus, the newly engineered cell line should be useful for the production of human GGT and as a potential alternative model for pharmacological studies.

Animals↗

Malondialdehyde adducts to, and fragmentation of, apolipoprotein B from human plasma.

Many recent in vitro experiments support the hypothesis that oxidatively modified low density lipoproteins (LDLs) could participate in atherogenesis. Oxidation of LDLs, especially derivatization by aldehydes originating from peroxidation of fatty acids and fragmentation of apolipoprotein (apo) B-100 which is their major apolipoprotein, probably occurs extravascularly and the presence of oxidized LDLs in the circulation is not well documented. Using electrophoresis and immunodetection techniques, we studied the structure of apo B and the presence of adducts of malondialdehyde (MDA) to this protein in LDLs from plasma of a limited population of five healthy subjects and nine patients with severe atherosclerosis. In the patient-derived LDLs, apo B appeared extensively fragmented, much more so than in those from the healthy subjects, although LDLs were isolated in all cases in the presence of antioxidants, protease inhibitors and antibiotics. Additionally, in all healthy subjects, we found a minor fragment of apo B-100, apo B-74, whereas the complementary peptide, apo B-26, was not detected; thus the presence of this minor form cannot be related to cleavage of apo B-100, either by proteolysis or by oxidation. We also present evidence that MDA adducts are present in circulating apo B and most of its fragments not only in atheromatous patients, but also in healthy subjects. Our results are consistent with the existence of oxidized LDLs in the human circulation. However, the role of non-oxidative phenomena in the structural modifications affecting apo B which are reported here cannot be excluded.

Adult↗

A method for the determination of UDP-glucuronosyltransferase activity toward arylcarboxylic acids.

A fast and reliable method for the assay of UDP-glucuronosyltransferase (UGT) activity toward aglycones containing a carboxylic acid function is described. The procedure involves incubation with UDP-[U-14C]-glucuronic acid, the common substrate for the reaction, solid-phase separation of the radiolabeled acylglucuronides and unreacted cofactor, and quantification by liquid scintillation counting. The technique was validated for each of the seven substrates tested by reversed-phase HPLC, and was then applied successfully to the determination of optimal conditions for the activation of the carboxylic acid-UGT, and the estimation of kinetic constants for the glucuronidation of clofibric acid, 2-naphthylacetic acid, naproxen, and 4,4,4-triphenylbutanoic acid in rat liver microsomes. From the results obtained, we believe that this is an assay which, with only minor modification, could be applied to a wide range of carboxylic acid substrates for which, until now, specific and sensitive assays have been largely unavailable.

Animals↗

A novel UDP-Glc-specific glucosyltransferase catalyzing the biosynthesis of 6-O-glucosides of bile acids in human liver microsomes.

Two active site-directed photoaffinity analogs, 5-[beta-32P]azido-UDP-glucuronic acid and 5-[beta-32P]azido-UDP-glucose, were used for the characterization of UDP-sugar-utilizing enzymes in human liver microsomes. Both compounds were recognized by human microsomal proteins: major photolabeled bands of 50-56 kDa were detected. Both photoincorporations were competitively decreased by increasing concentrations of either UDP-Glc or UDP-GlcUA, indicating a high affinity for both nucleotides. The patterns of photoaffinity labeling in the 50-56-kDa range by the two probes were significantly different, indicating the presence of different UDP-GlcUA- and UDP-Glc-specific enzymes of similar molecular mass. The presence of a UDP-Glc-dependent transferase was confirmed by the identification of an enzymatic activity catalyzing the formation of glucosides of the 6 alpha-hydroxylated bile acid hyodeoxycholic acid (3 alpha, 6 alpha-diOH (HDCA)) in the presence of UDP-Glc. The specific activity of 1.5-3.2 nmol/min/mg of protein was similar to that of 6 alpha-glucuronidation of HDCA. The apparent Km for UDP-Glc estimated with HDCA was 280 microM, and the formation of HDCA glucosides was strongly inhibited by UDP-GlcUA (apparent Ki = 7 microM). Evidence is presented that HDCA-specific UDP-glucuronosyltransferase (clone UGT2B4) expressed in V79 cells is not involved in glucosidation of HDCA and is not photolabeled with 5-[beta-32P]azido-UDP-Glc. Rigorous structure identification of the biosynthetic product proved that HDCA was glucosidated at the 6-position. Thus, this UDP-Glc-dependent activity catalyzing the biosynthesis of 6-O-glucosides of 6 alpha-hydroxylated bile acids represents a new pathway in the metabolism of these bile acids.

Adolescent↗

Differential effects of human recombinant interleukin-1 beta and dexamethasone on hepatic drug-metabolizing enzymes in male and female rats.

Interleukin-1 beta (IL-1) is one of the major inflammation mediators, commonly reported to be an inhibitor of hepatic drug metabolism. We studied the effect of IL-1 treatment on various drug-metabolizing enzymes in male and female rats. IL-1 induced both cytochrome P450 (P450) 3A1 activity and protein in females, but in males, IL-1 repressed P450 3A2 activity, without decreasing the protein. P450 1A1 was impaired in males, but was retained after dexamethasone pretreatment. IL-1 did not change P450 2B1/2 activity and protein, but counteracted their induction by dexamethasone. Uridine diphospho-glucuronosyltransferase (UGT) 1A2 (bilirubin) activity and its induction by dexamethasone were not affected by IL-1 treatment. Both P450 2C11 and epoxide hydrolase activities were repressed by IL-1 treatment, and both activities were impaired after dexamethasone treatment. These results clearly demonstrate that IL-1 acts at different steps of protein synthesis and gene expression. The effect of IL-1 on P450 was isoform-dependent, indicating that IL-1 can act on pretranscriptional events. The discrepancy between the variations of the activities and the protein of P450 3A2 suggests a post-translational regulation. For P450 2C11, 3A1, and for microsomal epoxide hydrolase, but not for P450 1A1 and 2B1/2, IL-1 mimics the glucocorticoid effects. These differential effects can affect the kinetics and the bioavailability of drugs used in pathologies in which IL-1 is increased.

Animals↗