Effects of L-carnitine supplementation on oxidative stress and antioxidant enzymes activities in patients with coronary artery disease: A randomized, placebo-controlled trial

Abstract

Background: Cardiovascular disease is the leading cause of death worldwide. Higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the effect of L-carnitine (LC, 1000 mg/d) on the markers of oxidative stress and antioxidant enzymes activities in CAD patients. Methods. We enrolled 47 CAD patients in the study. The CAD patients were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery. The subjects were randomly assigned to the placebo (n = 24) and LC (n = 23) groups. The intervention was administered for 12 weeks. The levels of serum LC, plasma malondialdehyde (MDA), and erythrocyte antioxidant enzymes activities [catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)] were measured before and after intervention. Results: Thirty-nine subjects completed the study (placebo, n = 19; LC, n = 20). After 12 weeks of LC supplementation, the level of MDA was significantly reduced (2.0 ± 0.3 to 1.8 ± 0.3 μmol/L, P = 0.02) and the level of LC (33.6 ± 13.6 to 40.0 ± 12.0 μmol/L, P = 0.04) and antioxidant enzymes activities [CAT (12.7 ± 5.5 to 13.1 ± 5.8 U/mg of protein, P = 0.02), SOD (14.8 ± 2.9 to 20.7 ± 5.8 U/mg of protein, P < 0.01), and GPx (20.3 ± 3.4 to 23.0 ± 3.1 U/mg of protein, P = 0.01)] were significantly increased. The level of LC was significantly positively correlated with the antioxidant enzymes activities (CAT, β = 0.87, P = 0.02; SOD, β = 0.72, P < 0.01). Conclusion: LC supplementation at a dose of 1000 mg/d was associated with a significant reduction in oxidative stress and an increase in antioxidant enzymes activities in CAD patients. CAD patients might benefit from using LC supplements to increase their anti-oxidation capacity. Trial registration. Clinical Trials.gov Identifier: NCT01819701.