Effects of captopril on cell damage and liver damage; [Kaptoprilin hücre hasarı ve karaciğer hasarı üzerine etkileri]

ArticleAçık Erişim

Özet

Objective: To evaluate the effects of captopril (CAP), an angiotensin converting enzyme inhibitor (ACEI), on oxidative stress, liver enzymes, cardiovascular damage, and micronucleus (MN) frequency in streptozotocin-induced diabetes mellitus (STZ-DM). Material and Methods: A total of 24 young Sprague-Dawley male rats were divided into three groups as control, STZ, and STZ+CAP. The rats with DM, induced by way of a single dose injection of STZ (45 mg/kg), received CAP 50 mg/L/day for eight weeks. At the end of this period, liver and cardiovascular damage was evaluated from the level of creatine kinase (CK), creatine kinase isoenzyme-MB (CK-MB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) and the level of lipid peroxidation was evaluated using the thiobarbituric acid reactive substances (TBARS), glu-tathione (GSH), and total thiol content (T-SH). The MN frequency was also examined. Results: STZ was found to cause significant increases in the TBARS and LDH levels, ALT and AST activity, and MN frequency and a decrease in the GSH levels, while CAP increased T-SH production and decreased LDH activity and MN frequency. However, CAP increased the activities of ALT and AST. Conclusion: Our study results suggest that CAP produces antioxidant effects in rats with STZ-induced DM and long-term use of CAP can correct the complications of diabetes at the cellular level, such as cell and tissue damage, as well as causing liver damage. Based on these results, diabetes seems to affect the liver, kidneys, and heart to varying degrees, although the liver is the most extensively affected organ. © 2020 by Türkiye Klinikleri.

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RDL Kalıcı Bağlantı (PID)
https://rdlopen.rawdatalibrary.net/r/ebyu/13779Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.5336/medsci.2020-74422Yayıncı resmi DOI adresi
Tam Kayıt
AlanDeğerDil
dc.contributor.authorÖner Gürsoy, Şule
dc.contributor.authorCeritli, Murat
dc.contributor.authorÜnüvar, Songül
dc.contributor.authorAktay, Göknur
dc.date.accessioned2026-10-18T20:28:35.764954534Z
dc.date.available2026-10-18T20:28:35.764954534Z
dc.date.issued2020
dc.description.abstractObjective: To evaluate the effects of captopril (CAP), an angiotensin converting enzyme inhibitor (ACEI), on oxidative stress, liver enzymes, cardiovascular damage, and micronucleus (MN) frequency in streptozotocin-induced diabetes mellitus (STZ-DM). Material and Methods: A total of 24 young Sprague-Dawley male rats were divided into three groups as control, STZ, and STZ+CAP. The rats with DM, induced by way of a single dose injection of STZ (45 mg/kg), received CAP 50 mg/L/day for eight weeks. At the end of this period, liver and cardiovascular damage was evaluated from the level of creatine kinase (CK), creatine kinase isoenzyme-MB (CK-MB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) and the level of lipid peroxidation was evaluated using the thiobarbituric acid reactive substances (TBARS), glu-tathione (GSH), and total thiol content (T-SH). The MN frequency was also examined. Results: STZ was found to cause significant increases in the TBARS and LDH levels, ALT and AST activity, and MN frequency and a decrease in the GSH levels, while CAP increased T-SH production and decreased LDH activity and MN frequency. However, CAP increased the activities of ALT and AST. Conclusion: Our study results suggest that CAP produces antioxidant effects in rats with STZ-induced DM and long-term use of CAP can correct the complications of diabetes at the cellular level, such as cell and tissue damage, as well as causing liver damage. Based on these results, diabetes seems to affect the liver, kidneys, and heart to varying degrees, although the liver is the most extensively affected organ. © 2020 by Türkiye Klinikleri.
dc.description.sponsorshipThe present study was supported by the University Scientific Research Projects Department (2009/02).
dc.identifier.doi10.5336/medsci.2020-74422
dc.identifier.eissn2146-9040
dc.identifier.endpage325
dc.identifier.issn1300-0292
dc.identifier.issue3
dc.identifier.scopus2-s2.0-85091657445
dc.identifier.startpage320
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13779
dc.identifier.volume40
dc.language.isotr
dc.publisherTurkiye Klinikleri
dc.relation.ispartofTurkiye Klinikleri Journal of Medical Sciences
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAngiotensin converting enzyme inhibitor
dc.subjectCaptopril
dc.subjectDiabetes mellitus
dc.subjectLiver damage
dc.subjectOxidative stress
dc.subjectalanine aminotransferase
dc.subjectantioxidant
dc.subjectaspartate aminotransferase
dc.subjectcreatine kinase
dc.subjectcreatine kinase isoenzyme
dc.subjectcreatine kinase MB
dc.subjectlactate dehydrogenase
dc.subjectmalonaldehyde
dc.subjectstreptozocin
dc.subjectthiobarbituric acid reactive substance
dc.subjectthiol
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectcell damage
dc.subjectdiabetic complication
dc.subjectenzyme activity
dc.subjectenzyme linked immunosorbent assay
dc.subjectgene expression
dc.subjectglucose blood level
dc.subjectheart injury
dc.subjectlipid peroxidation
dc.subjectliver injury
dc.subjectmale
dc.subjectnonhuman
dc.titleEffects of captopril on cell damage and liver damage; [Kaptoprilin hücre hasarı ve karaciğer hasarı üzerine etkileri]
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus1
rdl.citation.trdizin0
rdl.departmentİNÖNÜ ÜNİVERSİTESİ
rdl.departmentERZİNCAN BİNALİ YILDIRIM ÜNİVERSİTESİ
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexTRDIZIN