Thiol-Disulfide Homeostasis, Serum Ferroxidase Activity, and Serum Ischemia Modified Albumin Levels in Neonatal Jaundice

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Aim: Hyperbilirubinemia causes oxidative stress. Method: We evaluated three oxidative stress markers in hyperbilirubinemic neonates (native/total thiol levels, serum ferroxidase activity and ischemia modified albumin (IMA), comparing these levels to levels in a control group to determine which indicators were the most sensitive. Results: Serum from 124 term infants (67 with pathologic jaundice and 57 controls) were evaluated. Native/total thiol ratio was significantly lower (p:0.021) while disulfide levels were significantly higher (p:0.001) in the jaundiced group. There was no significant difference in ferroxidase (p:0.603) or IMA (p:0.251) levels. Conclusion: Altered thiol/disulfide homeostasis in the favor of disulfide indicates augmented oxidative stress in jaundiced term infants. The lack of alteration in ferroxidase or IMA levels suggests these latter alterations take more time or more severe oxidative stress to become altered or are not as sensitive as the thiol/disulfide ratio to detect oxidative stress states. © 2019, © 2019 Taylor & Francis Group, LLC.

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AlanDeğerDil
dc.contributor.authorTopal, Ismail
dc.contributor.authorMertoglu, Cuma
dc.contributor.authorSurucu Kara, Ilknur
dc.contributor.authorSiranli, Gulsah
dc.contributor.authorGok, Gamze
dc.contributor.authorErel, Özcan
dc.date.accessioned2026-10-18T20:28:32.924821197Z
dc.date.available2026-10-18T20:28:32.924821197Z
dc.date.issued2019
dc.description.abstractAim: Hyperbilirubinemia causes oxidative stress. Method: We evaluated three oxidative stress markers in hyperbilirubinemic neonates (native/total thiol levels, serum ferroxidase activity and ischemia modified albumin (IMA), comparing these levels to levels in a control group to determine which indicators were the most sensitive. Results: Serum from 124 term infants (67 with pathologic jaundice and 57 controls) were evaluated. Native/total thiol ratio was significantly lower (p:0.021) while disulfide levels were significantly higher (p:0.001) in the jaundiced group. There was no significant difference in ferroxidase (p:0.603) or IMA (p:0.251) levels. Conclusion: Altered thiol/disulfide homeostasis in the favor of disulfide indicates augmented oxidative stress in jaundiced term infants. The lack of alteration in ferroxidase or IMA levels suggests these latter alterations take more time or more severe oxidative stress to become altered or are not as sensitive as the thiol/disulfide ratio to detect oxidative stress states. © 2019, © 2019 Taylor & Francis Group, LLC.
dc.identifier.doi10.1080/15513815.2018.1561772
dc.identifier.eissn1551-3823
dc.identifier.endpage145
dc.identifier.issn1551-3815
dc.identifier.issue2
dc.identifier.pmid30741063
dc.identifier.scopus2-s2.0-85061429950
dc.identifier.startpage138
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13724
dc.identifier.volume38
dc.identifier.wosWOS:000469316800006
dc.language.isoen
dc.publisherTaylor and Francis Ltd
dc.relation.ispartofFetal and Pediatric Pathology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectferroxidase
dc.subjectischemia modified albumin
dc.subjectneonatal jaundice
dc.subjectthiol/disulfide homeostasis
dc.subjectBiomarkers
dc.subjectCeruloplasmin
dc.subjectDisulfides
dc.subjectHomeostasis
dc.subjectHumans
dc.subjectInfant
dc.subjectInfant, Newborn
dc.subjectJaundice, Neonatal
dc.subjectOxidative Stress
dc.subjectSerum Albumin
dc.subjectSerum Albumin, Human
dc.subjectSulfhydryl Compounds
dc.subjectbilirubin
dc.subjectdisulfide
dc.subjecthemoglobin
dc.subjectthiol derivative
dc.subjectthiol group
dc.subjectbiological marker
dc.subjecthuman serum albumin
dc.subjectischemia-modified albumin
dc.subjectArticle
dc.subjectblood group ABO incompatibility
dc.subjectceruloplasmin blood level
dc.subjectclinical evaluation
dc.subjectcomparative study
dc.subjectcontrolled study
dc.titleThiol-Disulfide Homeostasis, Serum Ferroxidase Activity, and Serum Ischemia Modified Albumin Levels in Neonatal Jaundice
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus7
rdl.citation.wos5
rdl.departmenta Pediatrics, Erzincan University Faculty of Medicine, Erzincan, Turkey. | b Clinical Biochemistry, Erzincan University Faculty of Medicine, Erzincan, Turkey.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)