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Abstract
Oxidative stress (OS) has been implicated in the pathophysiology of many neurological,
particularly neurodegenerative diseases. OS can cause cellular damage and subsequent
cell death because the reactive oxygen species (ROS) oxidize vital cellular components
such as lipids, proteins, and DNA. Moreover, the brain is exposed throughout life
to excitatory amino acids (such as glutamate), whose metabolism produces ROS, thereby
promoting excitotoxicity. Antioxidant defense mechanisms include removal of O(2),
scavenging of reactive oxygen/nitrogen species or their precursors, inhibition of
ROS formation, binding of metal ions needed for the catalysis of ROS generation and
up-regulation of endogenous antioxidant defenses. However, since our endogenous antioxidant
defenses are not always completely effective, and since exposure to damaging environmental
factors is increasing, it seems reasonable to propose that exogenous antioxidants
could be very effective in diminishing the cumulative effects of oxidative damage.
Antioxidants of widely varying chemical structures have been investigated as potential
therapeutic agents. However, the therapeutic use of most of these compounds is limited
since they do not cross the blood brain barrier (BBB). Although a few of them have
shown limited efficiency in animal models or in small clinical studies, none of the
currently available antioxidants have proven efficacious in a large-scale controlled
study. Therefore, any novel antioxidant molecules designed as potential neuroprotective
treatment in acute or chronic neurological disorders should have the mandatory prerequisite
that they can cross the BBB after systemic administration.