Relationships between serum bilirubins and production and conjugation of bilirubin

Muraca, Maurizio; Fevery, Johan; Blanckaert, Norbert

doi:10.1016/0016-5085(87)90123-5

Cited by 67 publications

(14 citation statements)

References 34 publications

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“…According to Koh et al (2012) the increase of urea concentrations in serum may be due to toxic effect towards liver function, as urea is the end product of protein catabolism. Increase in total bilirubin was observed in TBT treated animals which may be due to reduced liver uptake, conjugation or increased bilirubin production from hemolysis (Muraca et al 1987). Some of the essential functions of the liver include detoxification of bilirubin, epimerization of galactose to glucose as uridine-5-phosphate derivatives and synthesis of protein (albumin) and prothrombin.…”

Section: Discussionmentioning

confidence: 99%

Tributyltin-mediated hepatic, renal and testicular tissue damage in male Syrian hamster (Mesocricetus auratus): a study on impact of oxidative stress

et al. 2016

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Organotin compounds are a versatile group of organometallic chemicals that are used in a variety of industrial and agricultural applications. Tributyltin (TBT), a common organotin, brings about severe spermatotoxic and organotoxic effects. However, information about the adverse effects of TBT on liver, kidney and testis is scanty. Hence, the present study was undertaken to elucidate the TBT-mediated oxidative stress-induced impairments in these organs. Administration of TBT through oral route at increasing doses of 50, 100 and 150 ppm for 65 days to male Syrian hamsters resulted in drastically decreased activities of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase and decreased mean levels of non-enzymatic antioxidants (reduced glutathione, vitamin C, and vitamin E) followed by a dramatic increase in the levels of lipid peroxidation in the liver, kidney and testis as compared to the control animals. Significantly high levels of serum urea, creatinine, uric acid and bilirubin were observed in TBT-treated hamsters. Also, TBT treatment induced drastic histopathological changes in the liver, kidney and testis combined with remarkable changes in serum levels of tissue injury marker enzymes Aspartate transaminases, Alkaline phosphatase and Alanine transaminase. These data affirm that exposure to TBT can lead to oxidative stress-induced damage to liver, kidney and testis.

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Section: Discussionmentioning

confidence: 99%

Tributyltin-mediated hepatic, renal and testicular tissue damage in male Syrian hamster (Mesocricetus auratus): a study on impact of oxidative stress

et al. 2016

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“…Hepatic bilirubin glucuronosyltransferase activity is decreased in affected persons by 60-70% (26). Serum bilirubin fractions show a greater than normal unconjugated bilirubin fraction (Ͼ90%) (27) and a decreased diconjugated bilirubin component (17).…”

Section: Discussionmentioning

confidence: 99%

Gilbert syndrome and glucose-6-phosphate dehydrogenase deficiency: A dose-dependent genetic interaction crucial to neonatal hyperbilirubinemia

Kaplan

Renbaum

Levy‐Lahad

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

312

168

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Severe jaundice leading to kernicterus or death in the newborn is the most devastating consequence of glucose-6-phosphate dehydrogenase (EC 1.1.1.49; G-6-PD) deficiency. We asked whether the TA repeat promoter polymorphism in the gene for uridinediphosphoglucuronate glucuronosyltransferase 1 (EC 2.4.1.17; UDPGT1), associated with benign jaundice in adults (Gilbert syndrome), increases the incidence of neonatal hyperbilirubinemia in G-6-PD deficiency. DNA from term neonates was analyzed for UDPGT1 polymorphism (normal homozygotes, heterozygotes, variant homozygotes), and for G-6-PD Mediterranean deficiency. The variant UDPGT1 promoter allele frequency was similar in G-6-PD-deficient and normal neonates. Thirty (22.9%) G-6-PD deficient neonates developed serum total bilirubin > 257 mol͞liter, vs. 22 (9.2%) normals (P ‫؍‬ 0.0005). Of those with the normal homozygous UDPGT1 genotype, the incidence of hyperbilirubinemia was similar in G-6-PD-deficients and controls (9.7% and 9.9%). In contrast, in the G-6-PD-deficient neonates, those with the heterozygous or homozygous variant UDPGT1 genotype had a higher incidence of hyperbilirubinemia than corresponding controls (heterozygotes: 31.6% vs. 6.7%, P < 0.0001; variant homozygotes: 50% vs. 14.7%, P ‫؍‬ 0.02). Among G-6-PD-deficient infants the incidence of hyperbilirubinemia was greater in those with the heterozygous (31.6%, P ‫؍‬ 0.006) or variant homozygous (50%, P ‫؍‬ 0.003) UDPGT1 genotype than in normal homozygotes. In contrast, among those normal for G-6-PD, the UDPGT1 polymorphism had no significant effect (heterozygotes: 6.7%; variant homozygotes: 14.7%). Thus, neither G-6-PD deficiency nor the variant UDPGT1 promoter, alone, increased the incidence of hyperbilirubinemia, but both in combination did. This gene interaction may serve as a paradigm of the interaction of benign genetic polymorphisms in the causation of disease.

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“…The octyl (C8) column was shown to resolve UCB and MBR sufficiently whereas neither octadecyl (C18) nor phenylhexyl (C6-Phenyl) columns separated them (data not shown). The mobile phase contained TBA as an ion pair agent to ensure optimal peak sharpness and maximal sensitivity [10].…”

Section: Hplc Assaymentioning

confidence: 99%

“…Although a number of sensitive HPLC methods for bilirubin quantification in simple matrices like serum/plasma [10], bile [11], or microsomal preparations [12] have been established, different approaches are needed for the determination of bilirubin in complex tissues. Radioassay was used to assess brain and CSF bilirubin levels after intravenous administration of [ 14 C]-UCB to Gunn rats [13,14] and guinea pigs [13].…”

Section: Introductionmentioning

confidence: 99%

Highly sensitive method for quantitative determination of bilirubin in biological fluids and tissues

Zelenka

Leníček

Muchová

et al. 2008

Journal of Chromatography B

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Relationships between serum bilirubins and production and conjugation of bilirubin

Cited by 67 publications

References 34 publications

Tributyltin-mediated hepatic, renal and testicular tissue damage in male Syrian hamster (Mesocricetus auratus): a study on impact of oxidative stress

Tributyltin-mediated hepatic, renal and testicular tissue damage in male Syrian hamster (Mesocricetus auratus): a study on impact of oxidative stress

Gilbert syndrome and glucose-6-phosphate dehydrogenase deficiency: A dose-dependent genetic interaction crucial to neonatal hyperbilirubinemia

Highly sensitive method for quantitative determination of bilirubin in biological fluids and tissues

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