Reactive oxygen species mediate abnormal tau phosphorylation in a zinc-induced model [Bir Çinko-bazlı modelde reaktif oksijen grupları anormal tau fosforilasyona aracılık eder]

It has been well-established that amyloid-beta could induce reactive oxygen species (ros) overproduction and lead to oxidative stress whose end-productions surround hippocampal neurons in alzheimer's disease (ad) patients. in our previous study,it demonstrated that luteolin (lu) inhibited zinc-induced tau phosphorylation in an ros-dependent manner in human neuroblastoma sh-sy5y cells. in the current study,we further examined the effect of ros on tau phosphorylation and its possible underlying mechanism in this model. we found that incubation of cells with exogenous reduced glutathione resulted in abolishment of the elevation of tau phosphorylation at ser262/356. moreover,we have further investigated the effect of ros upon the inhibitory action of lu on tau hyperphosphorylation and it's a certain underlying mechanism. our data suggest (i) that inhibition of ros overproduction by gsh or lu recovers abnormal tau phosphorylation at ser262/356 epitope,in turn,the increase of intracellular ros by exogenous addition of h2o2 reverses the inhibitory effect of lu on tau phosphorylation; (ii) that h2o2 efficiently changes the expression of the protein phosphates 2a. © 2015,ege university press. all rights reserved.