Hydroxyl radical production in the substantia nigra after 6-hydroxydopamine and hypoxia-reoxygenation
Identifieur interne : 001E87 ( Main/Exploration ); précédent : 001E86; suivant : 001E88Hydroxyl radical production in the substantia nigra after 6-hydroxydopamine and hypoxia-reoxygenation
Auteurs : Federico A. Dajas-Bailador [Uruguay, Royaume-Uni] ; Anibal Martinez-Borges [Uruguay] ; Gustavo Costa [Uruguay] ; J. Andrés Abin [Uruguay] ; Emilia Martignoni [Italie] ; Giuseppe Nappi [Italie] ; Federico Dajas [Uruguay]Source :
- Brain Research [ 0006-8993 ] ; 1998.
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Abstract
To study the involvement of oxidative stress in 6-OHDA neurotoxicity, we investigated the production of the hydroxyl free radical (OH⋅) in the substantia nigra (SN) and the striatum (CS) several moments after intranigral injection of the neurotoxin, with or without an added episode of hypoxia (30 min, 95% N2, 5% O2). We utilized the hydroxylation of salicylate to 2,3 dihydroxybenzoic acid (2,3 DHBA) as indication of OH⋅ production. When 2.3 DHBA levels were not modified, the levels of 2,5 DHBA were taken as an indication of cytochrome P450 (CYP 450) metabolism. 6-OHDA alone did not increase the production of 2,3 DHBA in the SN. 2,5 DHBA increased significantly after 120 min and was high up to 24 h. An episode of hypoxia (60 min after 6-OHDA injection) significantly worsened the decrease of dopamine (DA) in the striatum assessed 8 days after injection of 6-OHDA in the SN. Hypoxia performed 60 min and 24 h before or 24 h after 6-OHDA did not show any additional effect on striatal DA levels. Contrary to results obtained after 6-OHDA alone, 2,3 DHBA increased significantly 120 min after the injection, when the hypoxia-reoxygenation was added to the 6-OHDA treatment. Our data are showing a relationship between the increase in OH⋅ production and a concomitant worsening of neuronal degeneration. As a whole, the results support the idea that neurons undergoing 6-OHDA neurotoxicity have their antioxidant defences affected and that oxidative stress is actually an important eliciting factor in 6-OHDA dependant neurodegeneration. However, OH⋅ may not be the main radical species involved in this process. Additionally, 6-OHDA also appeared to provoke a long-term increase in CYP 450 activity.
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DOI: 10.1016/S0006-8993(98)00989-5
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Andrés Abin</name><affiliation wicri:level="1"><country xml:lang="fr">Uruguay</country><wicri:regionArea>Neurochemistry Division, Instituto de Investigaciones Biológicas Clemente Estable, Avda Italia 3318, CP 11600 Montevideo</wicri:regionArea><wicri:noRegion>CP 11600 Montevideo</wicri:noRegion></affiliation></author><author><name sortKey="Martignoni, Emilia" sort="Martignoni, Emilia" uniqKey="Martignoni E" first="Emilia" last="Martignoni">Emilia Martignoni</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Fundazione `Istituto Neurologico Casimiro Mondino', Via Paleatro 3, 27100, Pavia</wicri:regionArea><wicri:noRegion>Pavia</wicri:noRegion></affiliation></author><author><name sortKey="Nappi, Giuseppe" sort="Nappi, Giuseppe" uniqKey="Nappi G" first="Giuseppe" last="Nappi">Giuseppe Nappi</name><affiliation wicri:level="1"><country xml:lang="fr">Italie</country><wicri:regionArea>Fundazione `Istituto Neurologico Casimiro Mondino', Via Paleatro 3, 27100, Pavia</wicri:regionArea><wicri:noRegion>Pavia</wicri:noRegion></affiliation></author><author><name sortKey="Dajas, Federico" sort="Dajas, Federico" uniqKey="Dajas F" first="Federico" last="Dajas">Federico Dajas</name><affiliation wicri:level="1"><country xml:lang="fr">Uruguay</country><wicri:regionArea>Neurochemistry Division, Instituto de Investigaciones Biológicas Clemente Estable, Avda Italia 3318, CP 11600 Montevideo</wicri:regionArea><wicri:noRegion>CP 11600 Montevideo</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">813</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="18">18</biblScope><biblScope unit="page" to="25">25</biblScope></imprint><idno type="ISSN">0006-8993</idno></series><idno type="istex">C743679D2860250C96616CD4076B1C275D819C33</idno><idno type="DOI">10.1016/S0006-8993(98)00989-5</idno><idno type="PII">S0006-8993(98)00989-5</idno><idno type="ArticleID">15034</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6-OHDA</term><term>Cytochrome P450</term><term>Disorders of the nervous system</term><term>Hydroxyl radical</term><term>Hypoxia</term><term>Neurotoxicity</term><term>Oxidative stress</term><term>Parkinson's disease</term><term>Substantia nigra</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To study the involvement of oxidative stress in 6-OHDA neurotoxicity, we investigated the production of the hydroxyl free radical (OH⋅) in the substantia nigra (SN) and the striatum (CS) several moments after intranigral injection of the neurotoxin, with or without an added episode of hypoxia (30 min, 95% N2, 5% O2). We utilized the hydroxylation of salicylate to 2,3 dihydroxybenzoic acid (2,3 DHBA) as indication of OH⋅ production. When 2.3 DHBA levels were not modified, the levels of 2,5 DHBA were taken as an indication of cytochrome P450 (CYP 450) metabolism. 6-OHDA alone did not increase the production of 2,3 DHBA in the SN. 2,5 DHBA increased significantly after 120 min and was high up to 24 h. An episode of hypoxia (60 min after 6-OHDA injection) significantly worsened the decrease of dopamine (DA) in the striatum assessed 8 days after injection of 6-OHDA in the SN. Hypoxia performed 60 min and 24 h before or 24 h after 6-OHDA did not show any additional effect on striatal DA levels. Contrary to results obtained after 6-OHDA alone, 2,3 DHBA increased significantly 120 min after the injection, when the hypoxia-reoxygenation was added to the 6-OHDA treatment. Our data are showing a relationship between the increase in OH⋅ production and a concomitant worsening of neuronal degeneration. As a whole, the results support the idea that neurons undergoing 6-OHDA neurotoxicity have their antioxidant defences affected and that oxidative stress is actually an important eliciting factor in 6-OHDA dependant neurodegeneration. However, OH⋅ may not be the main radical species involved in this process. Additionally, 6-OHDA also appeared to provoke a long-term increase in CYP 450 activity.</div></front></TEI><affiliations><list><country><li>Italie</li><li>Royaume-Uni</li><li>Uruguay</li></country></list><tree><country name="Uruguay"><noRegion><name sortKey="Dajas Bailador, Federico A" sort="Dajas Bailador, Federico A" uniqKey="Dajas Bailador F" first="Federico A" last="Dajas-Bailador">Federico A. Dajas-Bailador</name></noRegion><name sortKey="Abin, J Andres" sort="Abin, J Andres" uniqKey="Abin J" first="J. Andrés" last="Abin">J. 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