Alterations in the normal function of excitatory amino acid carrier 1 affect cysteine transport and GSH synthesis impairing zinc homeostasis (the thiol group of GSH can function as a principal Zn 2+ chelator for the maintenance of Zn 2+ homeostasis in neurons) and oxidative stress, enhancing susceptibility to ischemia-induced neuronal cell death in the hippocampus (162164)
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Additionally, OLE treatment, in a rat model of stroke by occlusion of the middle cerebral artery, induces a decrease of cerebral edema and plasma fibrinogen, inhibition of angiotensin converting enzyme (ACE) activity, and an increase of the antioxidant enzymes SOD, GPX, and catalase in brain tissue [223]
The chronic inflammation caused by autoimmune diseases can increase oxidative stress
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