ORIGINAL ARTICLE
Association of coronary artery disease severity and disulphide/native thiol ratio
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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, Turkey
3
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.
Publication date: 2017-04-06
Corresponding author
Bulent Bilir
Namik Kemal University School of Medicine, Department of Internal Medicine, Tekirdag,
Turkey.
Eur J Gen Med 2017;14(2):30-33
KEYWORDS
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.