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[Effect of carvedilol on antioxidative enzymatic defence in patients with stable angina]
Jan Kowalski1, Jan Błaszczyk, Tomasz Cegliński
1Katedra Rehabilitacji z Klinika Chorób Wewnetrznych i Rehabilitacji Kardiologicznej UM w Łodzi.
Insights
Carvedilol therapy improved antioxidant defenses in patients with stable angina. The drug increased superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px), and catalase (CAT) enzyme activities, aiding recovery.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Stable angina patients exhibit diminished antioxidative enzymatic defense.
- This reduction impacts the body's ability to combat oxidative stress.
Purpose of the Study:
- To investigate the effect of carvedilol on antioxidative enzymatic defense in stable angina patients.
- To assess changes in superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px), and catalase (CAT) activities.
Main Methods:
- 27 stable angina patients received escalating doses of carvedilol (12.5-50 mg/day).
- Erythrocyte SOD-1, GSH-Px, and CAT activities were measured pre-therapy and at 4, 8, and 12 weeks.
- A control group of 12 healthy subjects was included for comparison.
Main Results:
- Patients with stable angina showed significantly lower SOD-1, GSH-Px, and CAT activities compared to healthy controls.
- Carvedilol treatment led to a notable increase in all three enzyme activities.
- GSH-Px levels in patients approached those of healthy subjects after 8 and 12 weeks of therapy.
Conclusions:
- Carvedilol significantly enhances the antioxidative enzymatic defense system in patients with stable angina.
- The drug's ability to boost SOD-1, GSH-Px, and CAT suggests a protective role against oxidative stress in this patient group.
Abstract:
Effect of carvedilol on the antioxidative enzymatic defence was investigated in patients with stable angina. The study comprised 27 patients (20 men and 10 women), aged 38-55 years (mean 48.3 years) with stable angina. The patients were administered carvedilol in increasing every four weeks doses: 12.5 mg/day, 25 mg/day, 50 mg/day. The control group consisted of 12 healthy subjects aged 39-49 years (mean 45.7 years). Blood samples were collected before and 4, 8 and after 12 weeks of therapy in patients and once in control group. Our study has been approved by the local Ethics Committee. Superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px) and catalase (CAT) activities in erythrocytes were determined according to Misra and Fridovich, Little and O'Brien and Beers and Sizer; respectively. The enzymatic antioxidative defence was significantly decreased in patients with stable angina in comparison to healthy subjects. During carvedilol therapy an increase in SOD-1, GSH-Px and CAT activities was observed. Moreover GSH-Px activity after 8 and 12 weeks of carvedilol therapy did not differ from that observed in group of healthy subjects. The results of our study have shown that carvedilol enhances antioxidative enzymatic defence in patients with stable angina.
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