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| Articles
by
Hakan Ceyran |
Total Records (
1 ) for
Hakan Ceyran |
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Figen Narin
,
Nazmi Narin
,
Fatmagul Basarslan
,
Ali Baykan
,
Sadettin Sezer
,
Hulya Akgun
,
Aynur Akin
,
Mustafa Akcakus
and
Hakan Ceyran
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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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