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

Zelenka, Jaroslav; Leníček, Martin; Muchová, Lucie; Jirsa, M; Kudla, Michal; Balaz, Peter; Zadinová, M; Jd, Ostrow; Wong, Ruby M.; Vı́tek, Libor

doi:10.1016/j.jchromb.2008.03.005

Cited by 75 publications

(57 citation statements)

References 33 publications

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“…Tissue Bilirubin Quantification UCB content was determined on rapidly thawed samples using high-performance liquid chromatography with diode array detector (Agilent, Santa Clara, CA) as described (10). Briefly, 300 pmol of mesobilirubin in dimethylsulfoxide (internal standard) was added, and samples were homogenized on ice.…”

Section: Animal Sacrifice and Sample Collectionmentioning

confidence: 99%

“…The first aim of this work was to apply a sensitive, specific high-performance liquid chromatography method (10) to assess tissue UCB levels spontaneously present in Gunn (jj) rats with jaundice due to a homozygous mutation, leading to loss of function of bilirubin-UDP glucuronosyl transferase (UGT1A1), and their heterozygous (Jj) and wild-type (JJ) littermates. The second aim was to study serial changes in regional brain UCB levels when jj Gunn rats were treated with sulphadimethoxine to acutely displace UCB from albumin, mimicking the effects of acute increases in unconjugated hyperbilirubinemia that can occur in jaundiced newborns and patients with Crigler-Najjar type I.…”

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confidence: 99%

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Bilirubin accumulation and Cyp mRNA expression in selected brain regions of jaundiced Gunn rat pups

et al. 2012

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Section: Animal Sacrifice and Sample Collectionmentioning

confidence: 99%

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confidence: 99%

Bilirubin accumulation and Cyp mRNA expression in selected brain regions of jaundiced Gunn rat pups

et al. 2012

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“…Serum bilirubin levels were measured using a BNISTAT Bilirubinometer (Reichert Technologies, USA). Tissue extraction and bilirubin quantification for bilirubin measurement in the brain tissue were modified based on the assay published previously (18). In brief, the brain tissue (100 mg) was disintegrated to a fine suspension by grinding and subsequently diluted with extraction solvent: methanol/chloroform/n-hexane (63:31:6, v/v).…”

Section: Methodsmentioning

confidence: 99%

Developmental Onset of Bilirubin-induced Neurotoxicity Involves Toll-like Receptor 2-dependent Signaling in Humanized UDP-glucuronosyltransferase1 Mice

Yueh

Chen

Nguyen

et al. 2014

Journal of Biological Chemistry

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Background: Neonatal jaundice with dangerously high levels of serum bilirubin leads to neurological toxicity. Results: Toll-like receptor 2 signaling is essential for regulation of glia activation, neuroinflammation, and oxidative stress when neonatal mice experience severe hyperbilirubinemia. Conclusion: Toll-like receptor 2 signaling is linked to a protection mode against serum bilirubin-induced brain toxicity. Significance: Understanding how signaling from innate immunity contributes to bilirubin-induced pathology.

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“…Concentrations of biliary UCB and bilirubin-glucuronic acid conjugates in 2-month-old mice were determined by HPLC as previously described by Zelenka et al (2008) and by Spivak and Carey (1985), respectively.…”

Section: Bilirubin Measurementsmentioning

confidence: 99%

“…Quantitative determination of UCB in tissues of 2-monthold mice was performed as previously described by Zelenka et al (2008).…”

Section: Bilirubin Measurementsmentioning

confidence: 99%

Life-Long Correction of Hyperbilirubinemia with a Neonatal Liver-Specific AAV-Mediated Gene Transfer in a Lethal Mouse Model of Crigler–Najjar Syndrome

Bortolussi

Zentillin²,

Vaníková³

et al. 2014

Human Gene Therapy

104

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Null mutations in the UGT1A1 gene result in Crigler-Najjar syndrome type I (CNSI), characterized by severe hyperbilirubinemia and constant risk of developing neurological damage. Phototherapy treatment lowers plasma bilirubin levels, but its efficacy is limited and liver transplantation is required. To find alternative therapies, we applied AAV liver-specific gene therapy to a lethal mouse model of CNSI. We demonstrated that a single neonatal hUGT1A1 gene transfer was successful and the therapeutic effect lasted up to 17 months postinjection. The therapeutic effect was mediated by the presence of transcriptionally active double-stranded episomes. We also compared the efficacy of two different gene therapy approaches: liver versus skeletal muscle transgene expression. We observed that 5-8% of normal liver expression and activity levels were sufficient to significantly reduce bilirubin levels and maintain lifelong low plasma bilirubin concentration (3.1 -1.5 mg/dl). In contrast, skeletal muscle was not able to efficiently lower bilirubin (6.4 -2.0 mg/dl), despite 20-30% of hUgt1a1 expression levels, compared with normal liver. We propose that this remarkable difference in gene therapy efficacy could be related to the absence of the Mrp2 and Mrp3 transporters of conjugated bilirubin in muscle. Taken together, our data support the concept that liver is the best organ for efficient and long-term CNSI gene therapy, and suggest that the use of extra-hepatic tissues should be coupled to the presence of bilirubin transporters.

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

Cited by 75 publications

References 33 publications

Bilirubin accumulation and Cyp mRNA expression in selected brain regions of jaundiced Gunn rat pups

Bilirubin accumulation and Cyp mRNA expression in selected brain regions of jaundiced Gunn rat pups

Developmental Onset of Bilirubin-induced Neurotoxicity Involves Toll-like Receptor 2-dependent Signaling in Humanized UDP-glucuronosyltransferase1 Mice

Life-Long Correction of Hyperbilirubinemia with a Neonatal Liver-Specific AAV-Mediated Gene Transfer in a Lethal Mouse Model of Crigler–Najjar Syndrome

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