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dc.contributor.authorMehmetcik, G
dc.contributor.authorAykacToker, G
dc.contributor.authorUysal, M
dc.contributor.authorAlptekin, N
dc.date.accessioned2021-03-04T19:54:46Z
dc.date.available2021-03-04T19:54:46Z
dc.date.issued1997
dc.identifier.citationAlptekin N., Mehmetcik G., Uysal M., AykacToker G., "Evidence for oxidative stress in the hepatic mitochondria of bile duct ligated rats", PHARMACOLOGICAL RESEARCH, cilt.36, ss.243-247, 1997
dc.identifier.issn1043-6618
dc.identifier.otherav_921356a1-29b2-4c30-a31f-d557370ca74a
dc.identifier.othervv_1032021
dc.identifier.urihttp://hdl.handle.net/20.500.12627/98526
dc.identifier.urihttps://doi.org/10.1006/phrs.1997.0225
dc.description.abstractLipid peroxidation increased both in the liver homogenates and in the hepatic mitochondrial fraction of bile duct ligated (BDL)-rats. Although mitochondrial superoxide dismutase (SOD) activity did not change in the liver, glutathione (GSH) levels and glutathione peroxidase (GSH-Px) activity decreased in hepatic mitochondrial fraction of BDL-rats as compared to sham-operated rats. In addition, GSH-Px and glutathione transferase (GST) activities decreased but SOD activity remained unchanged in the post-mitochondrial fraction of the liver from BDL-rats. However, erythrocyte lipid peroxide and GSH levels did not change in BDL-rats. In conclusion, our results show that the disturbance of oxidant-antioxidant balance especially in mitochondria may be responsible for cholestatic injury in BDL-rats. (C) 1997 The Italian Pharmacological Society.
dc.language.isoeng
dc.subjectEczacılık
dc.subjectTemel Bilimler
dc.subjectTemel Eczacılık Bilimleri
dc.subjectYaşam Bilimleri
dc.subjectSağlık Bilimleri
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectFarmakoloji ve Toksikoloji
dc.subjectFARMAKOLOJİ VE ECZACILIK
dc.titleEvidence for oxidative stress in the hepatic mitochondria of bile duct ligated rats
dc.typeMakale
dc.relation.journalPHARMACOLOGICAL RESEARCH
dc.contributor.department, ,
dc.identifier.volume36
dc.identifier.issue3
dc.identifier.startpage243
dc.identifier.endpage247
dc.contributor.firstauthorID119407


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