Coaction of hepatic thioredoxin and glutathione systems in iron overload-induced oxidative stress

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dc.authoridBudak, Harun/0000-0002-7371-8959
dc.contributor.authorSonmez Aydin, Feyza
dc.contributor.authorHukkamli, Berna
dc.contributor.authorBudak, Harun
dc.date.accessioned2025-03-23T19:47:09Z
dc.date.available2025-03-23T19:47:09Z
dc.date.issued2021
dc.departmentSinop Üniversitesi
dc.description.abstractIn the present study, we demonstrate the coaction of thioredoxin and glutathione (GSH) systems in mouse liver against iron overload-induced oxidative stress (OS). Mice were injected intraperitoneally with an iron dextran solution twice a week for 3 weeks. Iron accumulation in mouse liver was demonstrated spectroscopically. To confirm the iron overload model in the liver, the increased gene expression levels of hepcidin (Hamp), ferroportin (Fpn1), and ferritin (Fth1), which regulate iron trafficking, were observed by a quantitative polymerase chain reaction. In the case of iron overload, the GSH level and the reduced glutathione/oxidized glutathione ratio, which represents a marker of OS, decreased significantly. An increase in the malondialdehyde level, one of the final products of the lipid peroxidation process, was observed. The gene expression of the thioredoxin system, including thioredoxin (Trx1) and thioredoxin reductase (TrxR1), was examined. Though TrxR1 expression decreased, no changes were observed in Trx1. The enzyme activity and semiquantitative protein expression of TRXR1 increased. The activity of GSH reductase and GSH peroxidase increased in the iron overload group. The gene and protein expressions of thioredoxininteracting protein, which is an indicator of the commitment of the cell to apoptosis, were elevated significantly. The increased protein expression of Bcl-2-related X protein and CASPASE-3, which is an indicator of apoptosis, increased significantly. In conclusion, excess iron accumulation in mouse liver tissue causes OS, which affects the redox state of the thioredoxin and GSH systems, inducing cell apoptosis and also ferroptosis due to increased lipid peroxidation and the depletion of GSH level.
dc.description.sponsorshipAtaturk University Scientific Research Projects Coordination Commission (ATAUNIBAP) [PRJ2016/151]
dc.description.sponsorshipAtaturk University Scientific Research Projects Coordination Commission (ATAUNIBAP), Grant/Award Number: PRJ2016/151
dc.identifier.doi10.1002/jbt.22704
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue4
dc.identifier.pmid33393188
dc.identifier.scopus2-s2.0-85099035708
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1002/jbt.22704
dc.identifier.urihttps://hdl.handle.net/11486/7297
dc.identifier.volume35
dc.identifier.wosWOS:000604262500001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Biochemical and Molecular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250323
dc.subjectglutathione system
dc.subjectiron overload
dc.subjectmouse liver
dc.subjectoxidative stress
dc.subjectthioredoxin system
dc.titleCoaction of hepatic thioredoxin and glutathione systems in iron overload-induced oxidative stress
dc.typeArticle

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