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The observed plasma increase in adenosine could be due to a decrease in adenosine deaminase activity, inhibition of adenosine kinase, or an increase in 5-nucleotidase, all of which can occur in the presence of oxidative stress [7072]

This was achieved by promoting early apoptosis via mitochondria-mediated cytochrome C-caspase activation and ROS-induced DNA damage pathways (105)

Loss of the mitochondrial electrochemical gradient impairs ATP production by the F 1 Fo ATP synthase and impairs neuronal energy metabolism [70,71,72]

Written informed consent was obtained from all of the patients

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