Paraquat induces oxidative stress, neuronal loss in substantia nigra region and Parkinsonism in adult rats: Neuroprotection and amelioration of symptoms by water-soluble formulation of Coenzyme Q10
Identifieur interne : 001E00 ( Main/Exploration ); précédent : 001D99; suivant : 001E01Paraquat induces oxidative stress, neuronal loss in substantia nigra region and Parkinsonism in adult rats: Neuroprotection and amelioration of symptoms by water-soluble formulation of Coenzyme Q10
Auteurs : Mallika Somayajulu-Ni U [Canada] ; Jagdeep K. Sandhu [Canada] ; Jerome Cohen [Canada] ; Marianna Sikorska [Canada] ; Ts Sridhar [Canada, Inde] ; Anca Matei [Canada] ; Henryk Borowy-Borowski [Canada] ; Siyaram Pandey [Canada]Source :
- BMC Neuroscience [ 1471-2202 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Cell Death, Immunohistochemistry, Locomotion, Male, Mesencephalon (metabolism), Mesencephalon (pathology), Neurons (metabolism), Oxidative Stress, Paraquat (poisoning), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (physiopathology), Rats, Rats, Long-Evans, Rotarod Performance Test, Tyrosine 3-Monooxygenase (metabolism), Ubiquinone (analogs & derivatives), Ubiquinone (therapeutic use), Vitamins (therapeutic use).
- MESH :
- chemical , analogs & derivatives : Ubiquinone.
- chemical , metabolism : Tyrosine 3-Monooxygenase.
- chemical , poisoning : Paraquat.
- chemically induced : Parkinson Disease, Secondary.
- drug therapy : Parkinson Disease, Secondary.
- metabolism : Mesencephalon, Neurons, Parkinson Disease, Secondary.
- pathology : Mesencephalon.
- physiopathology : Parkinson Disease, Secondary.
- chemical , therapeutic use : Ubiquinone, Vitamins.
- Animals, Cell Death, Immunohistochemistry, Locomotion, Male, Oxidative Stress, Rats, Rats, Long-Evans, Rotarod Performance Test.
Abstract
Parkinson's disease, for which currently there is no cure, develops as a result of progressive loss of dopamine neurons in the brain; thus, identification of any potential therapeutic intervention for disease management is of a great importance.
Here we report that prophylactic application of water-soluble formulation of coenzyme Q10 could effectively offset the effects of environmental neurotoxin paraquat, believed to be a contributing factor in the development of familial PD. In this study we utilized a model of paraquat-induced dopaminergic neurodegeneration in adult rats that received three weekly intra-peritoneal injections of the herbicide paraquat. Histological and biochemical analyses of rat brains revealed increased levels of oxidative stress markers and a loss of approximately 65% of dopamine neurons in the
Our data confirmed that paraquat-induced neurotoxicity represents a convenient rat model of Parkinsonian neurodegeneration suitable for mechanistic and neuroprotective studies. This is the first preclinical evaluation of a water-soluble coenzyme Q10 formulation showing the evidence of prophylactic neuroprotection at clinically relevant doses.
Url:
DOI: 10.1186/1471-2202-10-88
PubMed: 19635141
PubMed Central: 2724477
Affiliations:
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Le document en format XML
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<series><title level="j">BMC Neuroscience</title>
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<term>Cell Death</term>
<term>Immunohistochemistry</term>
<term>Locomotion</term>
<term>Male</term>
<term>Mesencephalon (metabolism)</term>
<term>Mesencephalon (pathology)</term>
<term>Neurons (metabolism)</term>
<term>Oxidative Stress</term>
<term>Paraquat (poisoning)</term>
<term>Parkinson Disease, Secondary (chemically induced)</term>
<term>Parkinson Disease, Secondary (drug therapy)</term>
<term>Parkinson Disease, Secondary (metabolism)</term>
<term>Parkinson Disease, Secondary (physiopathology)</term>
<term>Rats</term>
<term>Rats, Long-Evans</term>
<term>Rotarod Performance Test</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>Ubiquinone (analogs & derivatives)</term>
<term>Ubiquinone (therapeutic use)</term>
<term>Vitamins (therapeutic use)</term>
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<keywords scheme="MESH" type="chemical" qualifier="poisoning" xml:lang="en"><term>Paraquat</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term>
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<term>Neurons</term>
<term>Parkinson Disease, Secondary</term>
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<term>Cell Death</term>
<term>Immunohistochemistry</term>
<term>Locomotion</term>
<term>Male</term>
<term>Oxidative Stress</term>
<term>Rats</term>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Parkinson's disease, for which currently there is no cure, develops as a result of progressive loss of dopamine neurons in the brain; thus, identification of any potential therapeutic intervention for disease management is of a great importance.</p>
</sec>
<sec><title>Results</title>
<p>Here we report that prophylactic application of water-soluble formulation of coenzyme Q<sub>10 </sub>
could effectively offset the effects of environmental neurotoxin paraquat, believed to be a contributing factor in the development of familial PD. In this study we utilized a model of paraquat-induced dopaminergic neurodegeneration in adult rats that received three weekly intra-peritoneal injections of the herbicide paraquat. Histological and biochemical analyses of rat brains revealed increased levels of oxidative stress markers and a loss of approximately 65% of dopamine neurons in the <italic>substantia nigra </italic>
region. The paraquat-exposed rats also displayed impaired balancing skills on a slowly rotating drum (rotorod) evidenced by their reduced spontaneity in gait performance. In contrast, paraquat exposed rats receiving a water-soluble formulation of coenzyme Q<sub>10 </sub>
in their drinking water prior to and during the paraquat treatment neither developed neurodegeneration nor reduced rotorod performance and were indistinguishable from the control paraquat-untreated rats.</p>
</sec>
<sec><title>Conclusion</title>
<p>Our data confirmed that paraquat-induced neurotoxicity represents a convenient rat model of Parkinsonian neurodegeneration suitable for mechanistic and neuroprotective studies. This is the first preclinical evaluation of a water-soluble coenzyme Q<sub>10 </sub>
formulation showing the evidence of prophylactic neuroprotection at clinically relevant doses.</p>
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