Association of coronary artery disease severity and disulphide/native thiol ratio
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Bulent Bilir 1 * , Dursun Cayan Akkoyun 2, Murat Aydin 3, Demet Ozkaramanli-Gur 2, Hasan Degirmenci 4, Neslihan Albayrak 4, Aydın Akyuz 2, Seref Alpsoy 2, Cemile Koca 5, Ozcan Erel 5
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1 Namik Kemal University School of Medicine, Department of Internal Medicine, Tekirdag, Turkey.2 Namik Kemal University School of Medicine, Department of Cardiology, Tekirdag, Turkey3 Namik Kemal University School of Medicine, Department of Department of Biochemistry, Tekirdag, Turkey.4 Republic of Turkey Ministry of Health, State Hospital, Clinic of Cardiology, Tekirdag, Turkey.5 Yıldırım Beyazıt University School of Medicine, Department of Biochemistry, Ankara, Turkey.* Corresponding Author

Abstract

Introduction:
Oxidative stress is among the major components of cardiovascular disease pathogenesis. Thiols play a significant role in prevention of oxidative stress in the cell. The purpose of this study is to investigate the relationship between the severity of coronary artery disease and disulphide/native thiol ratio, also determine if this ratio can be used as a marker of oxidative stress in this population.

Material and Methods:
A total number of 107 patients with angiographically established coronary artery disease and 26 control subjects with normal coronary arteries were enrolled. The mean Gensini score of patients were calculated (mean=30) and a score of 29 or below was considered as mild and a score of 30 or higher coronary artery disease as severe. Serum total, native thiol was measured and the disulphide and disulphide/native thiol ratio were calculated as described by Erel&Neselioglu.

Results:
Patients with mild and severe coronary artery disease had significantly lower native thiol levels and higher disulphide/native thiol ratio levels when compared to the control subjects. Also severe disease’s disulphide/native thiol ratio were higher than mild.

Conclusions:
The increased disulphide/native thiol ratio related with the severity of coronary artery disease, may reflect the augmented oxidative stress in coronary artery disease.

Keywords

License

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Article Type: Original Article

EUR J GEN MED, Volume 14, Issue 2, April 2017, 30-33

https://doi.org/10.29333/ejgm/81878

Publication date: 06 Apr 2017

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Article Downloads: 1022

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