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The distribution of copper, zinc- and manganese-superoxide dismutase, and glutathione peroxidase messenger ribonucleic acid in rat basal ganglia. | LitMetric

The distribution of copper, zinc- and manganese-superoxide dismutase, and glutathione peroxidase messenger ribonucleic acid in rat basal ganglia.

Biochem Pharmacol

Neurodegenerative Diseases Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, Hodgkin Building, Guy's Campus, London, UK.

Published: March 2002

Oxidative stress may contribute to the progression of Parkinson's disease, and while the status of antioxidant enzymes is thus important, little data on their regional distribution in basal ganglia exist. We now report on the distribution and levels of messenger ribonucleic acid (m-RNA) for the antioxidant enzymes copper, zinc-superoxide dismutase (Cu,Zn-SOD), manganese-superoxide dismutase (Mn-SOD), and glutathione peroxidase in rat basal ganglia using in situ hybridisation histochemistry with complementary deoxyribonucleic acid probes specific for these enzymes. The m-RNA for Cu,Zn-SOD, Mn-SOD, and glutathione peroxidase was expressed throughout basal ganglia. Levels of m-RNA were significantly higher in substantia nigra pars compacta than in all other regions of basal ganglia for both Cu,Zn-SOD (53-62%, P<0.001) and Mn-SOD (37-45%, P<0.05). Mn-SOD m-RNA levels were also significantly higher in SN pars reticulata than in the nucleus accumbens (10%, P<0.05) and striatum (12%, P<0.01). In contrast, glutathione peroxidase m-RNA levels were only significantly higher in SN pars compacta when compared with SN pars reticulata (23%, P<0.05), and in the striatum when compared with the nucleus accumbens (21%, P<0.05). The data suggest that SN pars compacta may be vulnerable to oxidative stress and thus dependent on the high antioxidant capacity provided by these cytoprotective enzymes. In conclusion, this study demonstrates the relative distribution of antioxidant enzymes in rat basal ganglia and forms the basis for further study in rodent models of Parkinson's disease.

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http://dx.doi.org/10.1016/s0006-2952(01)00897-8DOI Listing

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