ParkinsonFranceV1, PascalFrancis, Curation, bibRecord, 001A80

Mitochondrial impairment as an early event in th process of apoptosis induced by glutathione depletion in neuronal cells : Relevance to Parkinson's disease

Identifieur interne : 001A80 ( PascalFrancis/Curation ); précédent : 001A79; suivant : 001A81

Mitochondrial impairment as an early event in th process of apoptosis induced by glutathione depletion in neuronal cells : Relevance to Parkinson's disease

Auteurs : M. Merad-Boudia [France] ; A. Nicole [France] ; D. Santiard-Baron [France] ; C. Saille [France] ; I. Ceballos-Picot [France]

Source :

Biochemical pharmacology [ 0006-2952 ] ; 1998.

RBID : Pascal:99-0003529

Descripteurs français

Pascal (Inist)
- Glutathion, Radical libre, Chaîne respiratoire, Parkinson maladie, Neurone, Stress oxydatif, Apoptose, Mort cellulaire, Mitochondrie, In vitro, Antioxydant, Prévention.

English descriptors

KwdEn :
- Antioxidant, Apoptosis, Cell death, Free radical, Glutathione, In vitro, Mitochondria, Neuron, Oxidative stress, Parkinson disease, Prevention, Respiratory chain.

Abstract

In Parkinson's disease (PD), dopaminergic cell death in the substantia nigra was associated with a profound glutathione (GSH) decrease and a mitochondrial dysfunction. The fall in GSH concentration seemed to appear before the mitochondrial impairment and the cellular death, suggesting that a link may exist between these events.The relationships between GSH depletion, reactive oxygen species (ROS) production, mitochondrial dysfunction and the mode of cell death in neuronal cells remain to be resolved and will provide important insights into the etiology of Parkinson's disease. An approach to determine the role of GSH in the mitochondrial function and in neurodegeneration was to create a selective depletion of GSH in a neuronal cell line in culture (NS20Y) by inhibiting its biosynthesis with L-buthionine(S,R)-sulfoximine (BSO), a specific inhibitor of γ-glutamylcysteine synthetase. This treatment led to a nearly complete GSH depletion after 24 hr and induced cellular death via an apoptotic pathway after 5 days of BSO treatment. By using the reactive oxygen species-sensitive probe 2',7'-dichlorofluorescin, we observed that the rapid GSH depletion was accompanied, early in the process, by a strong and transient intracellular increase in reactive oxygen species evidenced after I hr with BSO, culminating after 3 hr when the GSH level decreased to 30% of normal. GSH depletion induced a loss of mitochondrial function after 48 hr of BSO treatment. In particular, the activities of complexes I, II and IV of the respiratory chain were decreased by 32, 70 and 65%, respectively as compared to controls. These results showed the crucial role of GSH for maintaining the integrity of mitochondrial function in neuronal cells. Oxidative stress and mitochondrial impairment, preceding DNA fragmentation, could he early events in the apoptotic process induced by GSH depletion. Our data are consistent with the hypothesis that GSH depletion could contribute to neuronal apoptosis in Parkinson's disease through oxidative stress and mitochondrial dysfunction. BIOCHEM PHARMACOL 56;5: 645-655, 1998.

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<front><div type="abstract" xml:lang="en">In Parkinson's disease (PD), dopaminergic cell death in the substantia nigra was associated with a profound glutathione (GSH) decrease and a mitochondrial dysfunction. The fall in GSH concentration seemed to appear before the mitochondrial impairment and the cellular death, suggesting that a link may exist between these events.The relationships between GSH depletion, reactive oxygen species (ROS) production, mitochondrial dysfunction and the mode of cell death in neuronal cells remain to be resolved and will provide important insights into the etiology of Parkinson's disease. An approach to determine the role of GSH in the mitochondrial function and in neurodegeneration was to create a selective depletion of GSH in a neuronal cell line in culture (NS20Y) by inhibiting its biosynthesis with L-buthionine(S,R)-sulfoximine (BSO), a specific inhibitor of γ-glutamylcysteine synthetase. This treatment led to a nearly complete GSH depletion after 24 hr and induced cellular death via an apoptotic pathway after 5 days of BSO treatment. By using the reactive oxygen species-sensitive probe 2',7'-dichlorofluorescin, we observed that the rapid GSH depletion was accompanied, early in the process, by a strong and transient intracellular increase in reactive oxygen species evidenced after I hr with BSO, culminating after 3 hr when the GSH level decreased to 30% of normal. GSH depletion induced a loss of mitochondrial function after 48 hr of BSO treatment. In particular, the activities of complexes I, II and IV of the respiratory chain were decreased by 32, 70 and 65%, respectively as compared to controls. These results showed the crucial role of GSH for maintaining the integrity of mitochondrial function in neuronal cells. Oxidative stress and mitochondrial impairment, preceding DNA fragmentation, could he early events in the apoptotic process induced by GSH depletion. Our data are consistent with the hypothesis that GSH depletion could contribute to neuronal apoptosis in Parkinson's disease through oxidative stress and mitochondrial dysfunction. BIOCHEM PHARMACOL 56;5: 645-655, 1998.</div>
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</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Glutathione</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Glutatión</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Radical libre</s0>
<s2>FX</s2>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Free radical</s0>
<s2>FX</s2>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Radical libre</s0>
<s2>FX</s2>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Chaîne respiratoire</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Respiratory chain</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Cadena respiratoria</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Neurone</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Neuron</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Neurona</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Stress oxydatif</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Oxidative stress</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Stress oxidativo</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Apoptose</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Apoptosis</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Apoptosis</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Mort cellulaire</s0>
<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Cell death</s0>
<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Muerte celular</s0>
<s5>16</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Mitochondrie</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Mitochondria</s0>
<s5>17</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Mitocondria</s0>
<s5>17</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>In vitro</s0>
<s5>18</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>In vitro</s0>
<s5>18</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>In vitro</s0>
<s5>18</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Antioxydant</s0>
<s5>19</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Antioxidant</s0>
<s5>19</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Antioxidante</s0>
<s5>19</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Prévention</s0>
<s5>20</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Prevention</s0>
<s5>20</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Prevención</s0>
<s5>20</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>61</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>61</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>61</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>62</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>62</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>62</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>63</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>63</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>63</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>64</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>64</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>64</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>65</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>65</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>65</s5>
</fC07>
<fN21><s1>004</s1>
</fN21>
</pA>
</standard>
</inist>
</record>

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	La maladie de Parkinson en France (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

La maladie de Parkinson en France (serveur d'exploration)

Mitochondrial impairment as an early event in th process of apoptosis induced by glutathione depletion in neuronal cells : Relevance to Parkinson's disease

Mitochondrial impairment as an early event in th process of apoptosis induced by glutathione depletion in neuronal cells : Relevance to Parkinson's disease

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