Constitutional Nonhemolytic Hyperbilirubinemia in the Rat: Defect of Bilirubin Conjugation

Carbone, John V.; Grodsky, Gerold M.

doi:10.3181/00379727-94-22979

Cited by 108 publications

(31 citation statements)

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“…These findings differ from a recent report by Carbone and Grodsky (27), who stated that in jaundiced rats "glucuronyl transferase activity is absent or inhibited." The presence of a defect in glucuronide formation in these jaundiced rats had recently been confirmed by Lathe and Walker (28).…”

Section: Methodscontrasting

confidence: 57%

Congenital Jaundice in Rats, Due to a Defect in Glucuronide Formation1

Schmid¹,

Axelrod²,

Hammaker³

et al. 1958

J. Clin. Invest.

234

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Section: Methodscontrasting

confidence: 57%

Congenital Jaundice in Rats, Due to a Defect in Glucuronide Formation1

Schmid¹,

Axelrod²,

Hammaker³

et al. 1958

J. Clin. Invest.

234

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“…result of a deficiency in the hepatic microsomal enzyme, glucuronyl transferase, which catalyzes the conThe homozygous (jj) Gunn strain rat has a life-long jugation of bilirubin prior to hepatic excretion as the unconjugated hyperbilirubinemia which develops a diglucuronide ester [3,15,21]. few days after birth [11].…”

Section: Introductionmentioning

confidence: 99%

The Response of Jaundiced and Non-Jaundiced Weanling Rats to Thirsting

Odell

1968

Pediatr Res

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ExtractLitter-mate homozygous and heterozygous weanling rats of the Gunn strain were thirsted and fasted for 24 hours. The response of the animals to thirsting was compared by analysis of solute content of serum and composition of fluid in the renal medullae. The results are given in tables I and II. When the mean values for weight loss and serum solute concentrations were compared, it was found that the jaundiced rats were able to conserve body water as well as the non-jaundiced rats and to generate equally high concentrations of total solute in the tissue water of the renal medulla. Only two of the twelve jaundiced animals showed evidence of failure to develop the expected hypertonicity of the medullary tissue water. This failure was qualitatively similar to that found in adult jaundiced rats. Despite the presence of higher concentrations of bilirubin in serum, the medullary bilirubin content of the jaundiced weanling rat was only 5 % of the concentration found in adult animals. The sodium and urea concentrations in the renal medullary fluid were correlated (p <0.001) in the homozygous jaundiced rats (table IV and fig. 1). A similar correlation was not found in the non-jaundiced heterozygous animals. This finding suggests that the normal rat kidney has at least two mechanisms for renal transport of urea, one of which is sodium dependent and the other sodium independent and that the latter mechanism is inoperative in the jaundiced weanling rat. SpeculationIn vitro studies of bilirubin have previously suggested that toxicity is exerted by its surface activity on mitochondrial membranes. The examination of renal function in the intact jaundiced animal has revealed the possibility that tubular transport systems for urea and sodium are impaired in the presence of high concentrations of bilirubin in the renal medulla. These transport systems involve the maintenance of concentration gradients of sodium and urea across tubular epithelium. Bilirubin, through its surface activity, could impair the selective permeability of the membranes involved in urea and sodium transport within the renal medulla.

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“…groups beIn a third series of experiments (series III), we exd lie some-amined the controversial issue of whether homozygous Gunn rats, which are unable to form BMG (20,21), sed dual-la-can convert administered BMG to BDG by transgluctaining 3H uronidation (11,18). The animals were injected with glucurono-16-600 nmol of unlabeled or "4C-labeled BMG, with with a much the isotope in the tetrapyrrolic aglycone, and the BMG Mechanism of Bilirubin Diglucuronide Formation in Intact Rats and BDG excreted in bile were determined.…”

mentioning

confidence: 99%

Mechanism of Bilirubin Diglucuronide Formation in Intact Rats

Blanckaert¹,

Gollan²,

Schmid³

1980

J. Clin. Invest.

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A B S T R A C T Although it is well established that bilirubin monoglucuronide is formed in the liver from bilirubin by a microsomal bilirubin uridine diphosphate (UDP)-glucuronosyltransferase, the subcellular site of conversion of monoglucuronide to diglucuronide and the molecular mechanism involved in diglucuronide synthesis have not been identified. Based on in vitro studies, it has been proposed that two fundamentally different enzyme systems may be involved in diglucuronide synthesis in rat liver: (a) a microsomal UDP-glucuronosyltransferase system requiring UDPglucuronic acid as sugar donor or (b) a transglucuronidation mechanism that involves transfer ofa glucuronosyl residue from one monoglucuronide molecule to another, catalyzed by a liver plasma membrane enzyme. To clarify the mechanism by which bilirubin monoglucuronide is converted in vivo to diglucuronide, three different experimental approaches were used. First, normal rats were injected with either equal amounts of bilirubin-

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Constitutional Nonhemolytic Hyperbilirubinemia in the Rat: Defect of Bilirubin Conjugation

Cited by 108 publications

References 0 publications

Congenital Jaundice in Rats, Due to a Defect in Glucuronide Formation1

Congenital Jaundice in Rats, Due to a Defect in Glucuronide Formation1

The Response of Jaundiced and Non-Jaundiced Weanling Rats to Thirsting

Mechanism of Bilirubin Diglucuronide Formation in Intact Rats

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