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Mediators of Inflammation
Volume 2009, Article ID 391682, 7 pages
Research Article

The Interaction of Oxidative Stress Response with Cytokines in the Thyrotoxic Rat: Is There a Link?

1Division of Pediatric Rheumatology and Immunology, Department of Pediatrics, School of Medicine, Dokuz Eylul University, 35340 Inciralti, Izmir, Turkey
2Department of General Surgery, School of Medicine, Ege University, 35100 Izmir, Turkey
3Department of Biochemistry, School of Medicine, Adnan Menderes University, 09890 Aydin, Turkey
4Division of Endocrinology, Department of Internal Medicine, School of Medicine, Ege University, 35100 Izmir, Turkey

Received 28 September 2008; Revised 22 December 2008; Accepted 13 January 2009

Academic Editor: Sunit Kumar Singh

Copyright © 2009 Balahan Makay et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Oxidative stress is regarded as a pathogenic factor in hyperthyroidism. Our purpose was to determine the relationship between the oxidative stress and the inflammatory cytokines and to investigate how melatonin affects oxidative damage and cytokine response in thyrotoxic rats. Twenty-one rats were divided into three groups. Group A served as negative controls. Group B had untreated thyrotoxicosis, and Group C received melatonin. Serum malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), and nitric oxide derivates (N O x), and plasma IL-6, IL-10, and TNF-alpha were measured. MDA, GSH, N O x, IL-10, and TNF-alpha levels increased after L-thyroxine induction. An inhibition of triiodothyronine and thyroxine was detected, as a result of melatonin administration. MDA, GSH, and N O x levels were also affected by melatonin. Lowest TNF-alpha levels were observed in Group C. This study demonstrates that oxidative stress is related to cytokine response in the thyrotoxic rat. Melatonin treatment suppresses the hyperthyroidism-induced oxidative damage as well as TNF-alpha response.