Author： Russell R.L. Siedlak S.L. Raina A.K. Bautista J.M. Smith M.A. Perry G.
Publisher： Elsevier
ISSN： 0003-9861
Source： Archives of Biochemistry and Biophysics, Vol.370, Iss.2, 1999-10, pp. : 236-239
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Abstract
We analyzed glucose-6-phosphate dehydrogenase, the rate-controlling enzyme of the pentose phosphate pathway and free sulfhydryls, to study redox balance in Alzheimer disease. Glucose-6-phosphate dehydrogenase plays a pivotal role in homeostatic redox control by providing reducing equivalents to glutathione, the major nonenzymatic cellular antioxidant. There is a multitude of evidence that marks oxidative stress proximally in the natural history of Alzheimer disease. Consistent with a role for glutathione in defense against increased reactive oxygen, we found an upregulation of glucose-6-phosphate dehydrogenase together with increased sulfhydryls in Alzheimer disease. These data indicate that reductive compensation may play an important role in combating oxidative stress in Alzheimer disease.
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