Further evidence of altered redox status of hyperbilirubinaemic patients: Role of bilirubin in Gilbert syndrome

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Bilirubin is regarded as the most powerful endogenous antioxidant substance. It exhibits immunmodulator, inhibitor activities on kinases, yet it is clear that it can be potentially cytotoxic. Gilbert syndrome is characterised by hereditary, chronic, mild unconjugated hyperbilirubinaemia. 12 Gilbert syndrome patients and 15 healthy controls were investigated with special regard to reduction-oxidation status and free radical-antioxidant balance. Sera free SH-group concentration, H-donating ability, reducing power were measured spectrophotometric methods. Total scavenger capacity, describing free radical-antioxidant balance, was determined by a newly developed chemiluminometric method in sera, plasma and erythrocytes. Patients with Gilbert syndrome showed a significant increase of non-enzymatic antioxidant capacity. Elevated free SH-group concentration, H-donating ability and reducing power were found in mild hyperbilirubinaemia compared with control group patients. On the other hand no significant differences were detected regarding free radical-antioxidant balance in sera, plasma and erythrocytes between the groups. On the basis of these results it can be supposed that elevated bilirubin concentration, via indirect or compensatory way, strengthens non-enzymatic antioxidant capacity, without changes in antioxidant-free radical balance. That is why further investigations are needed to clarify the consequences of elevated bilirubin concentration on cell redox homeostasis.

Original languageEnglish
Pages (from-to)131-134
Number of pages4
JournalActa Biologica Szegediensis
Volume47
Issue number1-4
Publication statusPublished - 2003

Fingerprint

Gilbert Disease
bilirubin
Bilirubin
Oxidation-Reduction
Antioxidants
antioxidants
Free Radicals
hyperbilirubinemia
Hyperbilirubinemia
erythrocytes
Erythrocytes
Serum
Plasmas
homeostasis
phosphotransferases (kinases)
Homeostasis
Phosphotransferases
oxidation
Oxidation
Control Groups

Keywords

  • Free radical-antioxidant balance
  • Gilbert syndrome
  • Redox status
  • Total scavenger capacity

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Cell Biology
  • Neuroscience(all)
  • Applied Microbiology and Biotechnology

Cite this

@article{b833565b5aca4edc97e45b67b68a5a71,
title = "Further evidence of altered redox status of hyperbilirubinaemic patients: Role of bilirubin in Gilbert syndrome",
abstract = "Bilirubin is regarded as the most powerful endogenous antioxidant substance. It exhibits immunmodulator, inhibitor activities on kinases, yet it is clear that it can be potentially cytotoxic. Gilbert syndrome is characterised by hereditary, chronic, mild unconjugated hyperbilirubinaemia. 12 Gilbert syndrome patients and 15 healthy controls were investigated with special regard to reduction-oxidation status and free radical-antioxidant balance. Sera free SH-group concentration, H-donating ability, reducing power were measured spectrophotometric methods. Total scavenger capacity, describing free radical-antioxidant balance, was determined by a newly developed chemiluminometric method in sera, plasma and erythrocytes. Patients with Gilbert syndrome showed a significant increase of non-enzymatic antioxidant capacity. Elevated free SH-group concentration, H-donating ability and reducing power were found in mild hyperbilirubinaemia compared with control group patients. On the other hand no significant differences were detected regarding free radical-antioxidant balance in sera, plasma and erythrocytes between the groups. On the basis of these results it can be supposed that elevated bilirubin concentration, via indirect or compensatory way, strengthens non-enzymatic antioxidant capacity, without changes in antioxidant-free radical balance. That is why further investigations are needed to clarify the consequences of elevated bilirubin concentration on cell redox homeostasis.",
keywords = "Free radical-antioxidant balance, Gilbert syndrome, Redox status, Total scavenger capacity",
author = "K. Hagym{\'a}si and I. Kocsis and G. Lengyel and P{\'e}ter Sipos and J. Feh{\'e}r and A. Bl{\'a}zovics",
year = "2003",
language = "English",
volume = "47",
pages = "131--134",
journal = "Acta Biologica Szegediensis",
issn = "1588-385X",
publisher = "University of Szeged",
number = "1-4",

}

TY - JOUR

T1 - Further evidence of altered redox status of hyperbilirubinaemic patients

T2 - Role of bilirubin in Gilbert syndrome

AU - Hagymási, K.

AU - Kocsis, I.

AU - Lengyel, G.

AU - Sipos, Péter

AU - Fehér, J.

AU - Blázovics, A.

PY - 2003

Y1 - 2003

N2 - Bilirubin is regarded as the most powerful endogenous antioxidant substance. It exhibits immunmodulator, inhibitor activities on kinases, yet it is clear that it can be potentially cytotoxic. Gilbert syndrome is characterised by hereditary, chronic, mild unconjugated hyperbilirubinaemia. 12 Gilbert syndrome patients and 15 healthy controls were investigated with special regard to reduction-oxidation status and free radical-antioxidant balance. Sera free SH-group concentration, H-donating ability, reducing power were measured spectrophotometric methods. Total scavenger capacity, describing free radical-antioxidant balance, was determined by a newly developed chemiluminometric method in sera, plasma and erythrocytes. Patients with Gilbert syndrome showed a significant increase of non-enzymatic antioxidant capacity. Elevated free SH-group concentration, H-donating ability and reducing power were found in mild hyperbilirubinaemia compared with control group patients. On the other hand no significant differences were detected regarding free radical-antioxidant balance in sera, plasma and erythrocytes between the groups. On the basis of these results it can be supposed that elevated bilirubin concentration, via indirect or compensatory way, strengthens non-enzymatic antioxidant capacity, without changes in antioxidant-free radical balance. That is why further investigations are needed to clarify the consequences of elevated bilirubin concentration on cell redox homeostasis.

AB - Bilirubin is regarded as the most powerful endogenous antioxidant substance. It exhibits immunmodulator, inhibitor activities on kinases, yet it is clear that it can be potentially cytotoxic. Gilbert syndrome is characterised by hereditary, chronic, mild unconjugated hyperbilirubinaemia. 12 Gilbert syndrome patients and 15 healthy controls were investigated with special regard to reduction-oxidation status and free radical-antioxidant balance. Sera free SH-group concentration, H-donating ability, reducing power were measured spectrophotometric methods. Total scavenger capacity, describing free radical-antioxidant balance, was determined by a newly developed chemiluminometric method in sera, plasma and erythrocytes. Patients with Gilbert syndrome showed a significant increase of non-enzymatic antioxidant capacity. Elevated free SH-group concentration, H-donating ability and reducing power were found in mild hyperbilirubinaemia compared with control group patients. On the other hand no significant differences were detected regarding free radical-antioxidant balance in sera, plasma and erythrocytes between the groups. On the basis of these results it can be supposed that elevated bilirubin concentration, via indirect or compensatory way, strengthens non-enzymatic antioxidant capacity, without changes in antioxidant-free radical balance. That is why further investigations are needed to clarify the consequences of elevated bilirubin concentration on cell redox homeostasis.

KW - Free radical-antioxidant balance

KW - Gilbert syndrome

KW - Redox status

KW - Total scavenger capacity

UR - http://www.scopus.com/inward/record.url?scp=1342267473&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1342267473&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:1342267473

VL - 47

SP - 131

EP - 134

JO - Acta Biologica Szegediensis

JF - Acta Biologica Szegediensis

SN - 1588-385X

IS - 1-4

ER -