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Fırat Üniversitesi Sağlık Bilimleri Veteriner Dergisi
2006, Cilt 20, Sayı 1, Sayfa(lar) 009-013
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The Association Between Free Radical Damage and Transition Metals Cu and Fe in Humans with Chlamydiosis
Veteriner Kontrol ve Araştırma Enstitüsü, Elazığ – TÜRKİYE
Keywords: Chlamydiosis, Lipid peroxidation, Transition metals, Human, Serum

Chlamydiae are obligatory intracellular pathogens that cause many diseases of which the pathogenic mechanism are largely unknown. A free radical is defined as an atom or a molecule that has one or more unpaired electrons in one of its molecular orbital and they are produced by activated phagocytes as their bactericidal function. Lipid peroxidation is a significant threatining factor for cellular integrity and trace elements have significant effects on lipid peroxidation. Hydrogen peroxide is reduced by transition elements such as copper and iron (Fenton reaction) or by reacting with superoxide radicals (Haber-Weiss reaction) and thus hydroxil radicals are produced. Hydroxil radicals trigger lipid peroxidation.

This study was carried out to determine lipid peroxidation, the level of copper and iron and its association with lipid peroxidation in humans with chlamydiosis.

In this study, sera samples of 15 healthy subjects and 15 subjects found to be positive to chlamydia by CFT were used. Malondialdehyde was measured as indicator of lipid peroxidation, and levels of iron and copper were measured as transition metals.

When they were compared with the controls, it was observed that levels of lipid peroxid (p<0.001) and copper (p<0.05) in sera of infected humans increased but level of iron (p>0.05) remained unchanged.

As a result, levels of lipid peroxidation increased depending on increases reactive oxygen species during chlamydial infections. At the same time, levels of copper increased. There was no significant change at serum iron concentration. Superoxide dismutase (Cu-SOD) prevents toxication of free radicals and an increase in the level of this enzyme accompanies the destruction of the enzyme. Concomitant increase of Cu with increased lipid peroxidation can be explained as destruction of this enzyme.

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