Effects of captopril on cell damage and liver damage; [Kaptoprilin hücre hasarı ve karaciğer hasarı üzerine etkileri]
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.
Anahtar Kelimeler
Tam Kayıt
| Alan | Değer | Dil |
|---|---|---|
| dc.contributor.author | Öner Gürsoy, Şule | |
| dc.contributor.author | Ceritli, Murat | |
| dc.contributor.author | Ünüvar, Songül | |
| dc.contributor.author | Aktay, Göknur | |
| dc.date.accessioned | 2026-10-18T20:28:35.764954534Z | |
| dc.date.available | 2026-10-18T20:28:35.764954534Z | |
| dc.date.issued | 2020 | |
| dc.description.abstract | 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. | |
| dc.description.sponsorship | The present study was supported by the University Scientific Research Projects Department (2009/02). | |
| dc.identifier.doi | 10.5336/medsci.2020-74422 | |
| dc.identifier.eissn | 2146-9040 | |
| dc.identifier.endpage | 325 | |
| dc.identifier.issn | 1300-0292 | |
| dc.identifier.issue | 3 | |
| dc.identifier.scopus | 2-s2.0-85091657445 | |
| dc.identifier.startpage | 320 | |
| dc.identifier.uri | https://rdlopen.rawdatalibrary.net/r/ebyu/13779 | |
| dc.identifier.volume | 40 | |
| dc.language.iso | tr | |
| dc.publisher | Turkiye Klinikleri | |
| dc.relation.ispartof | Turkiye Klinikleri Journal of Medical Sciences | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | Angiotensin converting enzyme inhibitor | |
| dc.subject | Captopril | |
| dc.subject | Diabetes mellitus | |
| dc.subject | Liver damage | |
| dc.subject | Oxidative stress | |
| dc.subject | alanine aminotransferase | |
| dc.subject | antioxidant | |
| dc.subject | aspartate aminotransferase | |
| dc.subject | creatine kinase | |
| dc.subject | creatine kinase isoenzyme | |
| dc.subject | creatine kinase MB | |
| dc.subject | lactate dehydrogenase | |
| dc.subject | malonaldehyde | |
| dc.subject | streptozocin | |
| dc.subject | thiobarbituric acid reactive substance | |
| dc.subject | thiol | |
| dc.subject | animal experiment | |
| dc.subject | animal model | |
| dc.subject | Article | |
| dc.subject | cell damage | |
| dc.subject | diabetic complication | |
| dc.subject | enzyme activity | |
| dc.subject | enzyme linked immunosorbent assay | |
| dc.subject | gene expression | |
| dc.subject | glucose blood level | |
| dc.subject | heart injury | |
| dc.subject | lipid peroxidation | |
| dc.subject | liver injury | |
| dc.subject | male | |
| dc.subject | nonhuman | |
| dc.title | Effects of captopril on cell damage and liver damage; [Kaptoprilin hücre hasarı ve karaciğer hasarı üzerine etkileri] | |
| dc.type | Article | |
| dspace.entity.type | Publication | |
| rdl.citation.scopus | 1 | |
| rdl.citation.trdizin | 0 | |
| rdl.department | İNÖNÜ ÜNİVERSİTESİ | |
| rdl.department | ERZİNCAN BİNALİ YILDIRIM ÜNİVERSİTESİ | |
| rdl.oa.status | gold | |
| rdl.source.index | SCOPUS | |
| rdl.source.index | TRDIZIN |
