Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (MPP+) towards dopaminergic mesencephalic neurones in primary culture
Identifieur interne : 000B85 ( PascalFrancis/Corpus ); précédent : 000B84; suivant : 000B86Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (MPP+) towards dopaminergic mesencephalic neurones in primary culture
Auteurs : Sophie Callier ; Maryvonne Le Saux ; Anne-Marie Lhiaubet ; Thérèse Di Paolo ; William Rostene ; Didier PelapratSource :
- Journal of neurochemistry [ 0022-3042 ] ; 2002.
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Abstract
Recent findings suggest that gonadal steroid hormones are neuroprotective and may provide clinical benefits in delaying the development of Parkinson's disease. In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxy-dopamine or 1-methyl-4-phenylpyridinium ion (MPP+). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [3H]dopamine ([3H]DA) uptake, length of dopaminergic processes and lactate dehydrogenase (LDH) release measurement. In cultures grown in serum-supplemented medium, a 2-h pre-treatment with high concentrations (10-100 μM) of 17β-oestradiol or 17α-oestradiol, the stereoisomer with weak oestrogenic activity, protected both dopaminergic and non-dopaminergic neurones from toxicity induced by 6-hydroxydopamine (6-OHDA; 40 or 100 μM) and by the high MPP+ concentrations (50 μM) necessary to obtain significant neuronal death under those culture conditions. At these concentrations, MPP+ was no longer selective for dopaminergic neurones but affected all cells present in the culture. In contrast, the hormonal treatments did not protect against selective degeneration of dopaminergic neurones induced by lower MPP+ concentrations (below 10 μM), related to inhibition of complex I of respiratory chain. In cultures grown in serum-free medium, oestradiol concentrations higher than 1 μM induced neuronal degeneration and no protection against 6-OHDA or MPP+ toxicity was observed at lower concentrations of the steroid. The neuroprotective effects of 17a- or 17p-oestradiol evidenced in this model might be due to the antioxidant properties of these compounds. However, other non-genomic effects of the steroids cannot be excluded.
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Format Inist (serveur)
| NO : | PASCAL 02-0295171 INIST |
|---|---|
| ET : | Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (MPP+) towards dopaminergic mesencephalic neurones in primary culture |
| AU : | CALLIER (Sophie); LE SAUX (Maryvonne); LHIAUBET (Anne-Marie); DI PAOLO (Thérèse); ROSTENE (William); PELAPRAT (Didier) |
| AF : | Unité 339 INSERM. Hopital saint Antoine/Paris/France (1 aut., 2 aut., 3 aut., 5 aut., 6 aut.); Oncology and Molecular Endocrinology Research Center, Laval University Medical Center/Sainte Foy, Québec/Canada (1 aut., 4 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Etats-Unis; Da. 2002; Vol. 80; No. 2; Pp. 307-316; Bibl. 1 p.3/4 |
| LA : | Anglais |
| EA : | Recent findings suggest that gonadal steroid hormones are neuroprotective and may provide clinical benefits in delaying the development of Parkinson's disease. In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxy-dopamine or 1-methyl-4-phenylpyridinium ion (MPP+). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [3H]dopamine ([3H]DA) uptake, length of dopaminergic processes and lactate dehydrogenase (LDH) release measurement. In cultures grown in serum-supplemented medium, a 2-h pre-treatment with high concentrations (10-100 μM) of 17β-oestradiol or 17α-oestradiol, the stereoisomer with weak oestrogenic activity, protected both dopaminergic and non-dopaminergic neurones from toxicity induced by 6-hydroxydopamine (6-OHDA; 40 or 100 μM) and by the high MPP+ concentrations (50 μM) necessary to obtain significant neuronal death under those culture conditions. At these concentrations, MPP+ was no longer selective for dopaminergic neurones but affected all cells present in the culture. In contrast, the hormonal treatments did not protect against selective degeneration of dopaminergic neurones induced by lower MPP+ concentrations (below 10 μM), related to inhibition of complex I of respiratory chain. In cultures grown in serum-free medium, oestradiol concentrations higher than 1 μM induced neuronal degeneration and no protection against 6-OHDA or MPP+ toxicity was observed at lower concentrations of the steroid. The neuroprotective effects of 17a- or 17p-oestradiol evidenced in this model might be due to the antioxidant properties of these compounds. However, other non-genomic effects of the steroids cannot be excluded. |
| CC : | 002B02B10 |
| FD : | Mésencéphale; Neurone dopaminergique; Neurotoxine; Mort cellulaire; Neuroprotecteur; 17α-Oestradiol; 17β-Oestradiol; Antioxydant; In vitro; Animal; Parkinson maladie; Rat |
| FG : | Toxine; Oestrogène; Hormone stéroïde sexuelle; Hormone ovarienne; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata |
| ED : | Midbrain; Dopaminergic neuron; Neurotoxin; Cell death; Neuroprotective agent; 17α-Estradiol; 17β-Estradiol; Antioxidant; In vitro; Animal; Parkinson disease; Rat |
| EG : | Toxin; Estrogen; Sex steroid hormone; Ovarian hormone; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata |
| SD : | Mesencéfalo; Neurona dopaminérgica; Neurotoxina; Muerte celular; Neuroprotector; 17α-Estradiol; 17β-Estradiol; Antioxidante; In vitro; Animal; Parkinson enfermedad; Rata |
| LO : | INIST-4037.354000102175200110 |
| ID : | 02-0295171 |
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Hopital saint Antoine</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center</s1><s2>Sainte Foy, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Le Saux, Maryvonne" sort="Le Saux, Maryvonne" uniqKey="Le Saux M" first="Maryvonne" last="Le Saux">Maryvonne Le Saux</name><affiliation><inist:fA14 i1="01"><s1>Unité 339 INSERM. Hopital saint Antoine</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lhiaubet, Anne Marie" sort="Lhiaubet, Anne Marie" uniqKey="Lhiaubet A" first="Anne-Marie" last="Lhiaubet">Anne-Marie Lhiaubet</name><affiliation><inist:fA14 i1="01"><s1>Unité 339 INSERM. Hopital saint Antoine</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><affiliation><inist:fA14 i1="02"><s1>Oncology and Molecular Endocrinology Research Center, Laval University Medical Center</s1><s2>Sainte Foy, Québec</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Rostene, William" sort="Rostene, William" uniqKey="Rostene W" first="William" last="Rostene">William Rostene</name><affiliation><inist:fA14 i1="01"><s1>Unité 339 INSERM. Hopital saint Antoine</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Pelaprat, Didier" sort="Pelaprat, Didier" uniqKey="Pelaprat D" first="Didier" last="Pelaprat">Didier Pelaprat</name><affiliation><inist:fA14 i1="01"><s1>Unité 339 INSERM. Hopital saint Antoine</s1><s2>Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2002">2002</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>17α-Estradiol</term><term>17β-Estradiol</term><term>Animal</term><term>Antioxidant</term><term>Cell death</term><term>Dopaminergic neuron</term><term>In vitro</term><term>Midbrain</term><term>Neuroprotective agent</term><term>Neurotoxin</term><term>Parkinson disease</term><term>Rat</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Mésencéphale</term><term>Neurone dopaminergique</term><term>Neurotoxine</term><term>Mort cellulaire</term><term>Neuroprotecteur</term><term>17α-Oestradiol</term><term>17β-Oestradiol</term><term>Antioxydant</term><term>In vitro</term><term>Animal</term><term>Parkinson maladie</term><term>Rat</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Recent findings suggest that gonadal steroid hormones are neuroprotective and may provide clinical benefits in delaying the development of Parkinson's disease. In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxy-dopamine or 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [<sup>3</sup>H]dopamine ([<sup>3</sup>H]DA) uptake, length of dopaminergic processes and lactate dehydrogenase (LDH) release measurement. In cultures grown in serum-supplemented medium, a 2-h pre-treatment with high concentrations (10-100 μM) of 17β-oestradiol or 17α-oestradiol, the stereoisomer with weak oestrogenic activity, protected both dopaminergic and non-dopaminergic neurones from toxicity induced by 6-hydroxydopamine (6-OHDA; 40 or 100 μM) and by the high MPP<sup>+</sup> concentrations (50 μM) necessary to obtain significant neuronal death under those culture conditions. At these concentrations, MPP<sup>+</sup> was no longer selective for dopaminergic neurones but affected all cells present in the culture. In contrast, the hormonal treatments did not protect against selective degeneration of dopaminergic neurones induced by lower MPP<sup>+</sup> concentrations (below 10 μM), related to inhibition of complex I of respiratory chain. In cultures grown in serum-free medium, oestradiol concentrations higher than 1 μM induced neuronal degeneration and no protection against 6-OHDA or MPP<sup>+</sup> toxicity was observed at lower concentrations of the steroid. The neuroprotective effects of 17a- or 17p-oestradiol evidenced in this model might be due to the antioxidant properties of these compounds. However, other non-genomic effects of the steroids cannot be excluded.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>80</s2></fA05><fA06><s2>2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>) towards dopaminergic mesencephalic neurones in primary culture</s1></fA08><fA11 i1="01" i2="1"><s1>CALLIER (Sophie)</s1></fA11><fA11 i1="02" i2="1"><s1>LE SAUX (Maryvonne)</s1></fA11><fA11 i1="03" i2="1"><s1>LHIAUBET (Anne-Marie)</s1></fA11><fA11 i1="04" i2="1"><s1>DI PAOLO (Thérèse)</s1></fA11><fA11 i1="05" i2="1"><s1>ROSTENE (William)</s1></fA11><fA11 i1="06" i2="1"><s1>PELAPRAT (Didier)</s1></fA11><fA14 i1="01"><s1>Unité 339 INSERM. 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In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxy-dopamine or 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [<sup>3</sup>H]dopamine ([<sup>3</sup>H]DA) uptake, length of dopaminergic processes and lactate dehydrogenase (LDH) release measurement. In cultures grown in serum-supplemented medium, a 2-h pre-treatment with high concentrations (10-100 μM) of 17β-oestradiol or 17α-oestradiol, the stereoisomer with weak oestrogenic activity, protected both dopaminergic and non-dopaminergic neurones from toxicity induced by 6-hydroxydopamine (6-OHDA; 40 or 100 μM) and by the high MPP<sup>+</sup> concentrations (50 μM) necessary to obtain significant neuronal death under those culture conditions. At these concentrations, MPP<sup>+</sup> was no longer selective for dopaminergic neurones but affected all cells present in the culture. In contrast, the hormonal treatments did not protect against selective degeneration of dopaminergic neurones induced by lower MPP<sup>+</sup> concentrations (below 10 μM), related to inhibition of complex I of respiratory chain. In cultures grown in serum-free medium, oestradiol concentrations higher than 1 μM induced neuronal degeneration and no protection against 6-OHDA or MPP<sup>+</sup> toxicity was observed at lower concentrations of the steroid. The neuroprotective effects of 17a- or 17p-oestradiol evidenced in this model might be due to the antioxidant properties of these compounds. 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l="FRE"><s0>Oestrogène</s0><s5>35</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Estrogen</s0><s5>35</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Estrógeno</s0><s5>35</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Hormone stéroïde sexuelle</s0><s5>36</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Sex steroid hormone</s0><s5>36</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Hormona esteroide sexual</s0><s5>36</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Hormone ovarienne</s0><s5>37</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Ovarian hormone</s0><s5>37</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Hormona ovárica</s0><s5>37</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>45</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>45</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>45</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>46</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>46</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>46</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>47</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>47</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>47</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>48</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>48</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>48</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>49</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>49</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>49</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="12" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fN21><s1>169</s1></fN21></pA></standard><server><NO>PASCAL 02-0295171 INIST</NO><ET>Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>) towards dopaminergic mesencephalic neurones in primary culture</ET><AU>CALLIER (Sophie); LE SAUX (Maryvonne); LHIAUBET (Anne-Marie); DI PAOLO (Thérèse); ROSTENE (William); PELAPRAT (Didier)</AU><AF>Unité 339 INSERM. Hopital saint Antoine/Paris/France (1 aut., 2 aut., 3 aut., 5 aut., 6 aut.); Oncology and Molecular Endocrinology Research Center, Laval University Medical Center/Sainte Foy, Québec/Canada (1 aut., 4 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Journal of neurochemistry; ISSN 0022-3042; Coden JONRA9; Etats-Unis; Da. 2002; Vol. 80; No. 2; Pp. 307-316; Bibl. 1 p.3/4</SO><LA>Anglais</LA><EA>Recent findings suggest that gonadal steroid hormones are neuroprotective and may provide clinical benefits in delaying the development of Parkinson's disease. In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxy-dopamine or 1-methyl-4-phenylpyridinium ion (MPP<sup>+</sup>). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [<sup>3</sup>H]dopamine ([<sup>3</sup>H]DA) uptake, length of dopaminergic processes and lactate dehydrogenase (LDH) release measurement. In cultures grown in serum-supplemented medium, a 2-h pre-treatment with high concentrations (10-100 μM) of 17β-oestradiol or 17α-oestradiol, the stereoisomer with weak oestrogenic activity, protected both dopaminergic and non-dopaminergic neurones from toxicity induced by 6-hydroxydopamine (6-OHDA; 40 or 100 μM) and by the high MPP<sup>+</sup> concentrations (50 μM) necessary to obtain significant neuronal death under those culture conditions. At these concentrations, MPP<sup>+</sup> was no longer selective for dopaminergic neurones but affected all cells present in the culture. In contrast, the hormonal treatments did not protect against selective degeneration of dopaminergic neurones induced by lower MPP<sup>+</sup> concentrations (below 10 μM), related to inhibition of complex I of respiratory chain. In cultures grown in serum-free medium, oestradiol concentrations higher than 1 μM induced neuronal degeneration and no protection against 6-OHDA or MPP<sup>+</sup> toxicity was observed at lower concentrations of the steroid. The neuroprotective effects of 17a- or 17p-oestradiol evidenced in this model might be due to the antioxidant properties of these compounds. However, other non-genomic effects of the steroids cannot be excluded.</EA><CC>002B02B10</CC><FD>Mésencéphale; Neurone dopaminergique; Neurotoxine; Mort cellulaire; Neuroprotecteur; 17α-Oestradiol; 17β-Oestradiol; Antioxydant; In vitro; Animal; Parkinson maladie; Rat</FD><FG>Toxine; Oestrogène; Hormone stéroïde sexuelle; Hormone ovarienne; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Rodentia; Mammalia; Vertebrata</FG><ED>Midbrain; Dopaminergic neuron; Neurotoxin; Cell death; Neuroprotective agent; 17α-Estradiol; 17β-Estradiol; Antioxidant; In vitro; Animal; Parkinson disease; Rat</ED><EG>Toxin; Estrogen; Sex steroid hormone; Ovarian hormone; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Rodentia; Mammalia; Vertebrata</EG><SD>Mesencéfalo; Neurona dopaminérgica; Neurotoxina; Muerte celular; Neuroprotector; 17α-Estradiol; 17β-Estradiol; Antioxidante; In vitro; Animal; Parkinson enfermedad; Rata</SD><LO>INIST-4037.354000102175200110</LO><ID>02-0295171</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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