Neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease are characterized by the progressive deterioration of the structure and function of the nervous system. A number of environmental risk factors including potentially toxic elements such as iron, lead to negative effects on many metabolic reactions as well as neuroprotection. The aim of this study is to reveal whether long-term iron overload is one of the underlying factors in the pathogenesis of Alzheimer’s disease (AD).
15 young-adult male rats were randomly divided into 5 groups treated with iron through drinking water for 4 months. Following feeding, the iron content, reduced glutathione (GSH), and hydrogen peroxide (H2O2) levels of cortex tissues were measured. Specific enzyme activities were determined spectrophotometrically. mRNA expression profiles were measured using real-time PCR (qPCR).
Iron levels were elevated in case of non-toxic (0.87 and 3 μg/mL) iron administration. However, no changes were observed in toxic (30 and 300 μg/mL) iron administration. GSH and H2O2 levels altered with long-term iron overload. Glutathione peroxidase (GPx) enzyme activities signiﬁcantly increased in all groups, while glutathione S-transferase (GST) activity increased only in case of 0.87 and 30 μg/mL iron administration. Expression levels of neuroprotective and AD-related genes were altered by 3 μg/mL iron overload in a dose-dependent manner. The expression and activity of acetylcholinesterase (AChE) were elevated at 3 μg/mL iron concentration.
The findings of the present study allow us to conclude that long-term dietary iron intake, especially at a dose of 3 μg/mL demonstrates negative effects on the rat cortex by provoking antioxidant metabolism and AD pathology in a dose-dependently.