Oxidative stress induced-neurodegenerative diseases: the need for antioxidants that penetrate the blood brain barrier
Identifieur interne : 001959 ( Main/Exploration ); précédent : 001958; suivant : 001960Oxidative stress induced-neurodegenerative diseases: the need for antioxidants that penetrate the blood brain barrier
Auteurs : Yossi Gilgun-Sherki [Israël] ; Eldad Melamed [Israël] ; Daniel Offen [Israël]Source :
- Neuropharmacology [ 0028-3908 ] ; 2001.
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 O2, 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.
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DOI: 10.1016/S0028-3908(01)00019-3
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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 O2, 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.</div></front></TEI><affiliations><list><country><li>Israël</li></country></list><tree><country name="Israël"><noRegion><name sortKey="Gilgun Sherki, Yossi" sort="Gilgun Sherki, Yossi" uniqKey="Gilgun Sherki Y" first="Yossi" last="Gilgun-Sherki">Yossi Gilgun-Sherki</name></noRegion><name sortKey="Melamed, Eldad" sort="Melamed, Eldad" uniqKey="Melamed E" first="Eldad" last="Melamed">Eldad Melamed</name><name sortKey="Offen, Daniel" sort="Offen, Daniel" uniqKey="Offen D" first="Daniel" last="Offen">Daniel Offen</name><name sortKey="Offen, Daniel" sort="Offen, Daniel" uniqKey="Offen D" first="Daniel" last="Offen">Daniel Offen</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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