CHANGE OF ANTIOXIDANT ENZYME ACTIVITIES, SOME METALS AND LIPID PEROXIDATION IN ALZHEIMER’S DISEASE

AYŞE ARSLAN*, FATMA AYKAN TÜZÜN**, SIBEL TAMER***, HALIT DEMIR*, ABDURRAHMAN AYCAN****, CANAN DEMIR*****, MUHTEREM TASIN******, EDIP GÖNÜLLÜ*******

*Faculty of Science, Department of Biochemistry, Yuzuncu Yil University, Van, Turkey - **Private Kocaeli Hospital Center, Department of Neurology, Kocaeli, Turkey - ***Private Sincan Koru Hospital, Department of Neurology, Ankara, Turkey - ****Yuzuncu Yil University, Dursun Odabasi Research Hospital, Deparment of Brain Surgery, Van, Turkey - *****Yuzuncu Yil University, Vocational Schools of Health Services, Van, Turkey - ******Dicle University, Department of Neurology, Diyarbakir, Turkey - *******Training and Research Hospital, Department of Anesthesia, Van, Turkey

Introduction: Alzheimer’s disease (AD) is a neurodegenerative disease characterized by progressive cognitive regression and memory loss. It has been claimed that oxidative stress and factors such as metal accumulation in the brain play important roles in the etiopathogenesis of the disease.

Material and methods: The subjects of this study consisted of 24 individuals with Alzheimer's disease and 15 healthy agematched controls. Blood samples were withdrawn from the patients and healthy controls, and the activities of antioxidant enzymes SOD (Superoxide Dismutase), GSH (Glutathion), GSHPx (Glutathion peroxidase), GST (Glutathion S-Transferase) and MDA (Malondialdehyde) levels were determined by Spectrometer. Some metals and heavy metals were measured by atomic absorption spectrometry (AAS).

Results: Biochemical analyses showed a significant decrease of the main enzymatic antioxidant defences (SOD, GSH, GST and GSHPx) and increased production of lipid peroxidation marker (MDA) in the serum of AD patients, compared to age-matched control group (p<0.001). Also the levels of Zn, Mg, and Mn was lower and Fe, Pb, and Cd was higher in the patient group, compared to the control group. Serum Cu and Co levels did not differ significantly between the patient and control groups (p>0.001).

Conclusion: These results supports the theory that in AD there is a defect in the antioxidant defense system, which may lead to oxidative damage. Also alterations in some trace metals and their related enzymes may play a role of etiopathogenesis in AD.