The effect of L-tryptophan on the heart in rabbits via chronic hypoxia

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.

The effect of L-tryptophan on the heart in rabbits via chronic hypoxia

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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Turkish Journal of Medical Sciences-Cover
  • ISSN: 1300-0144
  • Yayın Aralığı: Yılda 6 Sayı
  • Yayıncı: TÜBİTAK
Sayıdaki Diğer Makaleler

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Cervical spine movement during intubation using the Airtraq® and direct laryngoscopy

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A bacteriological examination of urine before and after urodynamic testing

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