Diphosphate Glucuronyltransferase Activity Research Articles

Disease burden of Crigler-Najjar syndrome: Systematic review and future perspectives.

Crigler-Najjar syndrome (CNS) results from biallelic mutations of UGT1A1 causing partial or total loss of uridine 5'-diphosphate glucuronyltransferase activity leading to unconjugated hyperbilirubinemia and its attendant risk for irreversible neurological injury (kernicterus). CNS is exceedingly rare and has been only partially characterized through relatively small studies, each comprising between two and 57 patients. A systematic literature review was conducted to consolidate data on the patient, caregiver, and societal burden of CNS. Twenty-eight articles on clinical aspects of CNS were identified, but no published data on its humanistic or economic burden were found. In patients with complete UGT1A1 deficiency (type 1 CNS [CNS-I]), unconjugated bilirubin levels increase 3-6mg/dL/day during the newborn period and reach neurologically dangerous levels between 5 and 14days of age. Phototherapy is the mainstay of treatment but poses significant challenges to patients and their families. Despite consistent phototherapy, patients with CNS-I have worsening hyperbilirubinemia with advancing age. Liver transplantation is the only definitive therapy for CNS-I and is increasingly associated with excellent long-term survival but also incurs high costs, medical and surgical morbidities, and risks of immunosuppression. Crigler-Najjar syndrome is associated with a substantial burden, even with existing standards of care. The development of novel disease-modifying therapies has the potential to reduce disease burden and improve the lives of CNS patients and their families.

Explanted diseased livers - a possible source of metabolic competent primary human hepatocytes.

Being an integral part of basic, translational and clinical research, the demand for primary human hepatocytes (PHH) is continuously growing while the availability of tissue resection material for the isolation of metabolically competent PHH remains limited. To overcome current shortcomings, this study evaluated the use of explanted diseased organs from liver transplantation patients as a potential source of PHH. Therefore, PHH were isolated from resected surgical specimens (Rx-group; n = 60) and explanted diseased livers obtained from graft recipients with low labMELD-score (Ex-group; n = 5). Using established protocols PHH were subsequently cultured for a period of 7 days. The viability and metabolic competence of cultured PHH was assessed by the following parameters: morphology and cell count (CyQuant assay), albumin synthesis, urea production, AST-leakage, and phase I and II metabolism. Both groups were compared in terms of cell yield and metabolic function, and results were correlated with clinical parameters of tissue donors. Notably, cellular yields and viabilities were comparable between the Rx- and Ex-group and were 5.3±0.5 and 2.9±0.7×106 cells/g liver tissue with 84.3±1.3 and 76.0±8.6% viability, respectively. Moreover, PHH isolated from the Rx- or Ex-group did not differ in regards to loss of cell number in culture, albumin synthesis, urea production, AST-leakage, and phase I and II metabolism (measured by the 7-ethoxycoumarin-O-deethylase and uracil-5′-diphosphate-glucuronyltransferase activity). Likewise, basal transcript expressions of the CYP monooxygenases 1A1, 2C8 and 3A4 were comparable as was their induction when treated with a cocktail that consisted of 3-methylcholantren, rifampicin and phenobarbital, with increased expression of CYP 1A1 and 3A4 mRNA while transcript expression of CYP 2C8 was only marginally changed. In conclusion, the use of explanted diseased livers obtained from recipients with low labMELD-score might represent a valuable source of metabolically competent PHH which are comparable in viability and function to cells obtained from specimens following partial liver resection.

Pubertal exposure to thiodiazole copper inhibits thyroid function in juvenile female rats

Thiodiazole copper, as a thiadiazole fungicide, is widely used in China. The structure of thiodiazole copper shows a close relationship with N,N-methylene-bis (2-amino-1,3,4-thiadiazole) (Bis-A-TDA), which is a teratogen. A few studies have shown that some of the thiadiazole fungicides act as endocrine disruptors via disturbance in thyroid hormone homeostasis. Little is known about the effect of pubertal exposure to thiodiazole copper on the thyroid in pubertal female rats. Based on the protocol of the 20-day Pubertal Female Assay, we attempt to estimate the possible effects of exposure to thiodiazole copper on thyroid hormone and hepatic enzyme activity in female rats. Postnatal days (PND) 22-old Sprague–Dawley rats were administered with thiodiazole copper daily by oral gavage at doses 0, 4, 10, 20 or 30 mg/kg/day for 20 days. After treatments, the rats were sacrificed for blood collection; the reproductive organs, liver, pituitary, adrenal and thyroid gland were harvested. The results indicated that changes in thyroid endpoints following thiodiazole copper administration decreased serum triiodothyronine (T 3) and thyroxine (T 4) concentrations, increased thyroid stimulating hormone (TSH) concentrations and the weight of thyroid gland, induced hepatic uridine diphosphate glucuronyl transferase (UDPGT) activities in the highest dose group and produced thyroid gland hyperplasia. No histological changes were observed in uterus and ovaries moreover, age and weight at vaginal opening (VO) were unaffected by thiodiazole copper in all treatment groups. The absolute weights of liver and kidney were found to have decreased significantly in female rats. These data and changes demonstrate that thiodiazole copper is likely a thyroid disrupter in female rat following exposure during development, but doesnot have effect on the development of pubertal female rats. Further studies using environmentally relevant doses are needed for hazard identification.

Pubertal exposure to saisentong: Effects on thyroid and hepatic enzyme activity in juvenile female rats

Saisentong, as a thiadiazole fungicide, is widely used in China. The structure of saisentong shows a closer relationship to N, N-methylene-bis (2-amino-1, 3, 4-thiadiazole) (Bis-A-TDA), which is a teratogen. A few studies have shown that some of the thiadiazole fungicides act as endocrine disruptors via disturbance in thyroid hormone homeostasis. Little is known about the effect of pubertal exposure to saisentong on the development in pubertal female rats. Based on the protocol of the 20-Day Pubertal Female Assay, we attempt to estimate the possible effect of exposure to saisentong on thyroid hormone and hepatic enzyme activity in female rats. Postnatal days (PND) 22 old SD rats were administered with saisentong daily by oral gavage at doses of 0, 5, 10 or 15 mg/kg/day for 20 days. After treatment, the rats were sacrificed for blood collection; the reproductive organs, liver, pituitary, adrenal and thyroid gland were harvested. The results indicated that saisentong administration increased thyroid weight and thyroid stimulating hormone (TSH) concentrations, and induced hepatic uridine diphosphate glucuronyl transferase (UDPGT) activities in the highest-dose group, although not statistically significant. The high dose caused a decrease in weight at vaginal opening (VO), but the age at VO was unaffected by saisentong in all treatment groups. No histological changes were observed in uterus and ovaries. These data and changes demonstrate that saisentong is a potential thyroid disrupter in female rat following exposure during development, but does not affect the development of pubertal female rats.

Vitamin c and aloe vera supplementation protects from chemical hepatocarcinogenesis in the rat

The effects of vitamin C and aloe vera gel extract supplementation on induced hepatocarcinogenesis in male Sprague-Dawley rats (120-150 g) by diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) was investigated. The severity of the carcinogenesis process was determined by measuring gamma-glutamyl transpeptidase (GGT) and the placental form of glutathione S-transferase (GSTP) histochemically in situ and in plasma and liver fractions. In addition, plasma alkaline phosphatase (ALP) and liver microsomal uridine diphosphate glucuronyl transferase (UDPGT) activity were also determined. Administration of DEN/AAF caused an increase in the surface area and number of enzyme-positive foci (both GGT and GSTP) compared with control. Supplementation of vitamin C or aloe vera gel extract to the cancer-induced rats suppressed this increase significantly (P < 0.05; P < 0.001). Increases in liver UDPGT, GGT, and GSTP activities were also observed with cancer induction that were again suppressed with either vitamin C or aloe vera gel supplementation. Plasma GGT in the DEN/AAF rats were determined monthly for the duration of the experiment and found to be reduced as early as 1 mo with aloe vera gel supplementation and 2 mo with vitamin C supplementation. In conclusion, vitamin C and aloe vera gel extract supplementation were found to be able to reduce the severity of chemical hepatocarcinogenesis.

EFFECTS OF THE ESTROUS CYCLE AND THE GENDER DIFFERENCE ON HEPATIC DRUG-METABOLISING ENZYME ACTIVITIES

The aim of the present study was to investigate the effects of the estrous cycle and physiological dose of estradiol (E2) and the gender difference on several hepatic drug-metabolising enzyme activities. Eight-week old female Sprague-Dawley rats at different stages of the estrous cycle [proestrous (P), estrous (E), and diestrous (D)] and 8-week old male rats were used in this study (n=5, respectively). Serum E2level at D was higher than that at E and lower than that at P. The hepatic cytochrome P450 content, aniline hydroxylase, ethoxycoumarin O-deethylase and aminopyrineN-demethylase activities in male were significantly higher than those in female at any stage of the estrous cycle and these activities in female remained unchanged during the estrous cycle. Neither the estrous cycle nor the gender difference affected the cytochrome b5content. NADPH-cytochrome c reductase (fPT) activity at P was similar to that in male, and was significantly higher than that in E and D. fPTactivity was increased by the administration of physiological dose of E2in ovariectomized rats. Uridine diphosphate glucuronyltransferase (UDP-GT) activity at E was significantly lower than that at P or D and that activity in female was significantly lower than that in male. These results indicate that the estrous cycle, especially serum E2level, may affect both fPTand UDP-GT activities.

Determination by HPLC of the UDP-Glucuronyl Transferase Activity For 7-Hydroxycoumarin in Rabbit Tissue Samples

HPLC was used to determine the uridine diphosphate (UDP) glucuronyl transferase activity in rabbit tissues. The crude tissue samples prepared were from the liver, kidney, bladder, large intestine, lung, spleen, heart and fat. A metabolic reaction mixture was prepared that included the rabbit tissue sample, 7-hydroxycoumarin and UDP-glucuronic acid (UDPGA). The method was used to determine the level of production of 7-hydroxycoumarin-glucuronide from 7-hydroxycoumarin. Seperation of the analyte was carried out under gradient elution by reverse phase chromatography on a C18 column, with UV detection at 320 nm. It was possible to determine 7-hydroxycoumarin-glucuronide (7-OHCG) produced over time as well as the decrease in 7-hydroxycoumarin concentration as the reaction progressed. The rate of the reaction was calculated from a plot of the concentration of 7-OHCG produced versus time for each organ, and the rate calculated from the slope of the linear part of the curve. The liver showed the highest activity with a rate of production of 7-OHCG of 2.3 nmol per min per milligram of protein. The kidney showed an activity of 0.22 nmol of 7-OHCG produced per minute per milligram of protein, with the bladder and large intestine showing activities of 0.14 nmol and 7.8 pmol of 7-OHCG produced per minute per milligram of protein. The method used required minimal sample clean up and was reliable and accurate.

Is jaundice an early manifestation of Gilbert's syndrome in hypertrophic pyloric stenosis?

We report a case of congenital hypertrophic pyloric stenosis (HPS) associated with jaundice. The hepatic bilirubin uridine diphosphate glucuronyltransferase activity was low at the time of pylorotomy and 4 years later. In view of this observation, we discuss the significance of jaundice in HPS as a possible early manifestation of Gilbert's syndrome.

Species difference and tissue distribution of uridine diphosphate-glucuronyltransferase activities toward E6080, 1-naphthol and 4-hydroxybiphenyl.

The apparent in vitro kinetic constants of uridine diphosphate-glucuronyltransferase (UDP-GT) activities towards E6080, 1-naphthol (1-N) and 4-hydroxybiphenyl (4-HB) were determined using microsomes, to assess the effect of inducing agents and evaluate species and tissue differences. In rats, the 3-methylcholanthrene and beta-naphthoflavone treatments increased the Vmax app/KM app values for E6080, 13- and 8-fold, and those for 1-N, 1.9- and 1.7-fold, respectively, but did not affect those for 4-HB. Phenobarbital was ineffective on the UDP-GT activity toward E6080. In rats and rhesus monkeys, the intestinal mucosa had higher specific UDP-GT activity toward E6080 than did the liver, and the rank order of the Vmax app/KM app value for E6080 in the intestinal mucosa was rhesus monkey > rat > guinea pig > beagle. In guinea pig, the Vmax app/KM app value for E6080 in the liver was 4 times higher than that in the intestinal mucosa. Both the Vmax app/KM app values for 1-N and 4-HB in the liver of all species studied were higher than those in the intestinal mucosa, and guinea pig liver showed the highest values, while, about the Vmax app for 1-N and 4-HB, beagle liver had the highest values. In the beagle intestinal mucosa, the Vmax app/KM app values for all 3 substrates studied were extremely low.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucuronidation of mono(2-ethylhexyl)phthalate: Some enzyme characteristics and inhibition by bilirubin

A method for assaying mono(2-ethylhexyl)phthalate (MEHP) uridine diphosphate (UDP) glucuronyl transferase activity in microsomal preparations from guinea pig liver is described. The quantitation of the MEHP-glucuronide was performed by HPLC after direct injection of a sample of deproteinized incubation mixture. Solubilization of microsomal UDP-glucuronyltransferase activity was achieved by use of Lubrol, and optimal conditions for glucuronidation of MEHP were established. To investigate whether there is competition between MEHP and bilirubin for glucuronidation, inhibition experiments were performed with solubilized enzyme preparations. In these incubations addition of bilirubin decreased the formation of MEHP-glucuronide. No change in the maximal conversion rate ( V max) was observed, indicating the occurrence of competitive inhibition. This observation may have implications in clinical situations where patients with hyperbilirubinemia are exposed to MEHP, e.g. in exchange transfusions in newborn infants.

Species difference in codeine uridine diphosphate-glucuronyltransferase activity of liver microsomes.

Species difference in codeine uridine diphosphate-glucuronyltransferase (UDPGT) activity was studied in liver microsomes of mice, rats, guinea pigs and rabbits. Codeine UDPGT activity was the highest in guinea pigs, followed by that in rabbits, and the lowest in mice and rats among these four animal species. The specific activities of codeine UDPGT in liver microsomes were not correlated well with those toward morphine, 4-nitrophenol, and 4-hydroxybiphenyl in liver microsomes of each of the species. Inducibility of liver microsomal codeine UDPGT activity in rats was examined by pretreatment with phenobarbital and 3-methylcholanthrene and compared with those of other UDPGT activities. The activity was inducible by phenobarbital pretreatment as the activity toward morphine and 4-hydroxybiphenyl. The inducibility of codeine UDPGT activity by phenobarbital pretreatment was not as high as that of morphine UDPGT activity.

In vivo effects of tetrahydrocannabinols and their eight monooxygenated metabolites of the hepatic microsomal drug-metabolizing enzyme systems of mice.

In vivo effects of tetrahydrocannabinols (THCs) and their eight monooxygenated metabolites on the hepatic microsomal drug-metabolizing enzymes in mice were studied. delta 8-THC and its metabolites (7 alpha-hydroxy-, 7 beta-hydroxy- and 7-oxo-delta 8-THC, and 8 alpha, 9 alpha- and 8 beta, 9 beta-epoxyhexahydrocannabinol) tended to increase the enzyme contents or activities except for 7 beta-hydroxy-delta 8-THC which affected the microsomal enzymes in a different manner between the single and subchronic treatments. Single administration (5 mg/kg, i.v.) of 7-oxo-delta 8-THC, 8 alpha, 9 alpha- and 8 beta, 9 beta-epoxyhexahydrocannabinol led to the significant increase in hepatic microsomal p-nitroanisole O-demethylase and aniline hydroxylase activities accompanying a significant increase in cytochrome P-450 content in hepatic microsomes. The same results were obtained with subchronic treatment of mice with these metabolites (5 mg/kg/d, i.v. for 7 d), although the effect of 8 beta, 9 beta-epoxyhexahydrocannabinol on cytochrome P-450 was not statistically significant. 7 beta-Hydroxy-delta 8-THC significantly increased nicotinamide adenine dinucleotide phosphate (NADPH)-cytochrome c reductase and aniline hydroxylase activities by single administration, while the metabolite significantly decreased the contents of cytochrome b5 and P-450 and p-nitrophenol uridine diphosphate-glucuronyltransferase activity by the subchronic treatment. In contrast, delta 9-THC and its metabolites (8 alpha-hydroxy-, 8 beta-hydroxy- and 8-oxo-delta 9-THC) did not significantly affect the microsomal enzymes by both treatments except that the single administration of 8 alpha-hydroxy-delta 9-THC and the subchronic treatment of delta 9-THC significantly decreased NADPH-cytochrome c reductase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of o-Benzyl- p-chlorophenol on drug-metabolizing enzymes in rats

o-Benzyl- p-chlorophenol (BCP) is widely used as a broad spectrum disinfectant. Treatment of male Fischer 344 rats with BCP resulted in an increase in cytochrome P-450 content and an accompanying decrease in aryl hydrocarbon hydroxylase (AHH) activity in both liver and kidney microsomes. Several other drug-metabolizing enzymes were not affected by BCP treatment. However, in kidney, BCP induced NADPH-cytochrome c reductase and uridine diphosphate glucuronyl transferase activities and caused a small increase in total cytochrome P-450 content and glutathione concentration. The cytochrome P-450 isozymes induced by BCP were fractionated by high pressure liquid chromatography (HPLC). The HPLC profile following BCP treatment most closely resembled that seen after phenobarbital. Using an immunoblotting procedure and a radioimmunoassay, it was shown that the increase in cytochrome P-450 content in the liver after BCP treatment was, in part, due to an increase in the phenobarbital-inducible isozymes, P-450b + e. In the kidney, the increase in total cytochrome P-450 content after BCP exposure was not due to an increase in P-450b + e. The decrease in AHH activity appeared to be caused by noncompetitive inhibition of constitutive AHH activity by BCP. BCP also inhibited benzphetamine demethylation, although to a lesser extent. The failure to observe an increase in benzphetamine demethylase activity in vivo, despite the induction of P-450b, was probably due to the concomitant induction and inhibition of drug-metabolizing enzymes by BCP.

Conjugation and maximal biliary excretion of bilirubin in the rat during pregnancy and lactation and during estroprogestogen treatment.

Hepatic bilirubin conjugation and excretion were investigated during pregnancy and lactation in the rat. Bilirubin uridine diphosphate-glucuronyltransferase activity was decreased by 30% in pregnant rats, both when expressed per milligram of protein or as specific activity and per unit of liver weight. Liver size increased during pregnancy, and, as a consequence, total hepatic glucuronyltransferase activity was unchanged. The biliary bilirubin output was normal in pregnant rats, and when loaded with bilirubin, the maximal output in bile for the whole liver was also normal. In lactating rats, specific glucuronyltransferase activity returned to control values, but the activity per unit of liver weight was still lower, due to the decreased hepatic protein concentration. The liver remained enlarged during lactation, and total hepatic glucuronyltransferase activity was increased, together with the maximal output of bilirubin in bile. Two weeks after delivery, hepatic bilirubin conjugation and excretion in nonlactating mothers were comparable to those of virgin females. Parallel modifications of bilirubin glucuronyltransferase assayed in vitro and of maximal biliary output of the pigment in vivo were observed in all animals studied. The output of bilirubin diconjugates in bile was decreased during pregnancy but no changes of the proportion of the mono-to diconjugates in bile were observed 2 weeks after delivery both in lactating and in nonlactating rats. The modifications observed during pregnancy could not be reproduced by treatment with beta-estradiol and progesterone. This suggests that different hormones or modifications of steroid metabolism are probably involved in the alterations of hepatic bilirubin metabolism in pregnant and lactating rats.

Enhancement by secretin of the apparently maximal hepatic transport of bilirubin in the rat.

The effect of secretin (0.4 C.U. per hr per 100 gm body weight) on bile flow and the apparent maximal hepatic transport of bilirubin (Tm) was investigated in the rat. When secretin was administered during an already established bilirubin-Tm condition, it increased bile flow and bilirubin-Tm by 15 to 20% over a 30- to 50-min period. Enhancement of bilirubin output correlated with augmented flow and was sustained by an increased rate of excretion of monoglucuronides. When secretin was given for 90 min before bilirubin loading, it enhanced biliary bilirubin concentration and output, largely as diglucuronides. Bilirubin-Tm correlated positively with glururonyltransferase activity in liver homogenates. In the isolated perfused rat liver, injection of secretin in the portal cannula failed to produce choleresis. Bilirubin uridine diphosphate-glucuronyltransferase activity was lower than in intact rats and higher after treatment than in controls. The effect of secretin had an early effect on hepatocytic bile flow and a later effect on conjugation. Maximal hepatic bilirubin output was modulated both by flow and conjugation rate; the two mechanism may act independently.

Hepatic Billrubin-IX-alpha-Glycosyltransferase Activities in Animals Excreting Primarily Biliverdin into Bile.

A wide variation was observed in hepatic bilirubin-IX-alpha uridine diphosphate (UDP) glucuronyl, glucosyl and xylosyl transferase activities among yellow rat snakes, pin fish, chickens, turkeys, sea turtles, alligators, nutria and rats. Lower hepatic enzyme activities were observed in fish, snakes, turtles, and avian species with intermediate enzyme activities present in the livers of nutria and alligators. Hepatic glycosyltransferase activities were greater in the biliverdin-excreting species which are known to excrete readily an exogenous bilirubin load. Hepatic enzyme activities and the biliary transport maxima of bilirubin-IX-alpha are closely correlated.

Postnatal development of uridine diphosphate glucuronyltransferase activity towards bilirubin and 2-aminophenol in human liver.

UDP-glucuronyltransferase activities towards 2-aminophenol and bilirubin were studied in a total of 70 human subjects, including premature and full-term newborn babies, infants, children and adults. These two activities have been reported in rat to develop latefoetally and neonatally respectively, but in man they both develop neonatally. There is a linear relationship between the logarithm of each liver transferase activity and the logarithm of the number of days after birth during the first 3 months of life, after which each activity remains constant.

Stimulation of defective Gunn-rat liver uridine diphosphate glucuronyltransferase activity in vitro by alkyl ketones.

Addition of alkyl ketone (10mM) to Gunn-rat liver homogenates increased UDP-glucuronyltransferase activity towards 2-aminophenol by 10--20 fold, up to enhanced values of enzyme activity observed with similarly treated Wistar-rat liver homogenates. Alkyl ketones also activate the defective enzyme purified from Gunn-rat liver. This genetic deficiency of UDP-glucuronyltransferase activity is no longer apparent when assayed in the presence of alkyl ketones.

Augmentation of uridine diphosphate glucuronyltransferase activity in rat liver by adenosine 3′,5′-monophosphate

The role of cyclic adenosine 3′,5′-monophosphate (cAMP) in the regulation of rat liver bilirubin uridine diphosphate glucuronyltransferase (UDP-GT) was studied. Augmentation of UDP-GT activity was obtained by cAMP, but not by 3′-AMP. A single administration of glucagon initiated a rapid but limited increase in enzyme activity, which reached a maximum after 2 hr. Similar augmentation of the hepatic enzyme was produced by injection of N6,O2-dibutyryl cAMP. The nucleotide is the mediator for UDP-GT augmentation by glucagon. The injection of glucagon led within 20 min to a 40-fold increase in the concentration of cAMP. The augmentation of UDP-GT activity by glucagon or dibutyryl cAMP was fully inhibited by actinomycin D. A second stimulation of liver by glucagon or dibutyryl cAMP 4 hr after the first injection, produced a new increase of UDP-GT activity.

Differential Stimulation of Foetal Rat Liver Uridine Diphosphate Glucuronyltransferase Activity towards Certain Substrates after Glucocorticoid Treatment in Culture and in utero, and during Natural Development

Conference Article| June 01 1977 Differential Stimulation of Foetal Rat Liver Uridine Diphosphate Glucuronyltransferase Activity towards Certain Substrates after Glucocorticoid Treatment in Culture and in utero, and during Natural Development GRAHAM J. WISHART; GRAHAM J. WISHART 1Department of Biochemistry, University of Dundee, Dundee DD1 4HN, Scotland, U.K. Search for other works by this author on: This Site PubMed Google Scholar S. MOSSMAN; S. MOSSMAN 2Department of Biochemistry, University of Dundee, Dundee DD1 4HN, Scotland, U.K. Search for other works by this author on: This Site PubMed Google Scholar AGNES DONALD; AGNES DONALD 3Department of Biochemistry, University of Dundee, Dundee DD1 4HN, Scotland, U.K. Search for other works by this author on: This Site PubMed Google Scholar G. J. DUTTON G. J. DUTTON 4Department of Biochemistry, University of Dundee, Dundee DD1 4HN, Scotland, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1977) 5 (3): 721–723. https://doi.org/10.1042/bst0050721 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation GRAHAM J. WISHART, S. MOSSMAN, AGNES DONALD, G. J. DUTTON; Differential Stimulation of Foetal Rat Liver Uridine Diphosphate Glucuronyltransferase Activity towards Certain Substrates after Glucocorticoid Treatment in Culture and in utero, and during Natural Development. Biochem Soc Trans 1 June 1977; 5 (3): 721–723. doi: https://doi.org/10.1042/bst0050721 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1977 Biochemical Society1977 Article PDF first page preview Close Modal You do not currently have access to this content.