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Reactive oxygen species have been linked to neurodegenerative disease such as Alzheimer’s and Parkinson’s disease. Glucose-6-phosphate dehydrogenase (G6PD) is important for its role in the regeneration of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH). This reduced form is critical for maintaining glutathione (GSH) in its reduced form, which is essential for detoxification of reactive free radicals and lipid hydroperoxides. So far, the primary recognized health risk from common deficiencies in glucose-6-phosphate dehydrogenase (G6PD), a cytoprotective enzyme for oxidative stress, is red blood cell hemolysis. Our lab has recently shown in G6PD-deficient mice that G6PD is a developmentally critical cytoprotective enzyme for both endogenous and xenobiotic-initiated embryopathic oxidative stress and DNA damage and we have evidence that G6PD also protects against endogenous reactive oxygen species (ROS)-mediated neurodegeneration associated with aging. The objective of this work is to further characterize the role of G6PD as a neuroprotective enzyme. The activity of G6PD in 7 brain areas was measured using a spectrophotometric assay. The brain areas included the olfactory bulb, cortex, brain stem, striatum, substania nigra, hippocampus and cerebellum. The brains of G6PD-normal, heterozygous (+/-) G6PD-deficient and homozygous (-/-) G6PD-deficient mice were micro-dissected and the activity of G6PD was determined in these brain areas. This information will be used to further guide research into the neuroprotective role of G6PD. Since G6PD is the most common human enzymopathy, affecting over 400 million people world wide, this research may determine G6PD-deficiency as another determinant of neurodegenerative disease.
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