Pathogenesis of ischemic brain injury is occurred by crucial metabolic reasons. For instance, oxidative stress from free radical generation is causing to the thrombotic cerebrovascular stroke. In this case, the measurement of the oxidative stress is very important for a better understanding of the stroke pathophysiology. Because, the oxidative stress in stroke is generally assumed as one of the mechanisms taking part in neuronal damage. Thus, oxidative stress has a vital role in the cholinergic system.

We performed on 18 adult patients with stroke and 24 healthy persons as control subjects. First, acetylcholinesterase (AChE) activity and oxidative status were assayed in plasma and subsequently, quantitative gene expression of acetylcholinesterase was determined in leukocytes of patients diagnosed with acute stage of ischemia.

It was observed an increase in levels of the protein carbonyl content compared to the control (p=0.0011, p<0.01). The amount of the total thiol was lower than in the control groups of the ischemic patients (p=0.023, p<0.05). AChE and GST activities were significantly lower than control (p<0.01) in acute ischemic patients (p<0.01). mRNA expression of AChE was higher in the control groups than in the leukocytes of acute ischemic patients (p<0.05).

These results suggest that oxidative status, AChE activity and its gene expression were changed significantly at the acute ischemic patients.