Figen Narin, Nazmi Narin, Fatmagul Basarslan, Ali Baykan, Sadettin Sezer, Hulya Akgun, Aynur Akin, Mustafa Akcakus and Hakan Ceyran
Turkish Journal of Medical Sciences, 2010, 40(2), 257-263. DOI: 10.3906/sag-0901-4
Aim: To evaluate the protective effect of tryptophan on an experimentally
produced hypoxic myocardial injury via biochemical and pathological parameters.
Materials and methods: A total of 26 rabbits were divided into 3 groups. Group 1 (n = 9) was only exposed to hypoxia. Group 2 (n = 10) was exposed to hypoxia and received L-tryptophan (200 mg/kg per day, orally for 5 days). Group 3 (n = 7) was the control group. Before the hypoxic injury and after the delivery of the medication, serum samples were taken for troponin-I, creatine kinase myocardial isoenzymes (CK-MB), lactate dehydrogenase (LDH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), malondialdehyde (MDA), and nitric oxide (NO) analysis, and then the rabbits were sacrificed. Next, the myocardium samples were taken and the myocardial NO, MDA, SOD, and GSH-Px enzyme activity levels were studied histopathologically.
Results: In group 1, Serum GSH-Px and SOD activities were decreased. Conversely, troponin-I, CK-MB, and LDH were elevated. Severe cardiac injury was observed histopathologically. In group 2, serum troponin-I and SOD values were increased. Mild cardiac injury was demonstrated histopathologically. When groups 1 and 2 were compared, tissue NO and MDA levels in group 1 were higher compared to group 2, but GSH-Px level was found decreased in group 1.
Conclusion: Our findings support that there is a clear effect of the free oxygen radicals and the lipid peroxidation products on hypoxic cardiac injury. In addition, L-tryptophan supplementation has a strong protective effect on hypoxic heart by antioxidant activity.
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