The Effects of Different Antioxidants on the Activity of Cerebrocortical MnSOD and Na,K-ATPase from post mortem Alzheimer’s Disease and Age-matched Normal Brains
C. Kairane, R. Mahlapuu, K. Ehrlich, M. Zilmer and U. Soomets
Affiliation: Department of Biochemistry, Faculty of Medicine, University of Tartu, The Centre of Excellence of Translational Medicine, Ravila Str. 19, Tartu, 50411, Estonia.
Among the markers and targets of the early phase of Alzheimer’s disease (AD) pathogenesis MnSOD (mitochondrial
dysfunction) and Na-pump (disturbances in function/regulation) are often highlighted. This paper focused on
comparison of the effects of three antioxidants on the activity of cerebrocortical MnSOD and Na,K-ATPase from post
mortem Alzheimer’s disease and age-matched normal brains. Antioxidant compounds with different origins: natural glutathione,
synthetic UPF peptides (glutathione analogues) and phytoestrogen genistein were investigated. Firstly, MnSOD
and Na,K-ATPase activities were found to be decreased in the post mortem AD brains compared with age-matched controls.
Secondly, GSH had no effect on MnSOD activity, but decreased Na,K-ATPase activity both in the control and AD
brains. Thirdly, UPF1 and UPF17 increased MnSOD activity, and UPF17 suppressed Na,K-ATPase activity. Further studies
are needed to clarify, if the inhibitory effect of UPF17 on Na,K-ATPase could abolish the beneficial effect gained from
MnSOD activation. Both the antioxidative potential of genistein and its potency to up-regulate Na,K-ATPase activity
make it an attractive candidate substance to suppress the early phase of the pathogenesis of AD.
Keywords: Alzheimer's disease, genistein, MnSOD, Na, K-ATPase, oxidative stress, UPF peptides.
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