Involvement of Reactive Oxygen Species in a Feed-forward Mechanism of Na/K-ATPase-mediated Signaling Transduction

Puerarin induces the upregulation of glutathione levels and nuclear translocation of Nrf2 through PI3K/Akt/GSK-3β signaling events in PC12 cells exposed to lead

“…The brain is particularly vulnerable to oxidative damage because of its high energy requirements, high oxygen consumption, and relatively low levels of some antioxidant systems (reviewed by Ikonomidou and Kaindl, 2011). ROS are necessary for normal cellular functions such as signaling and synaptic plasticity (Yan et al, 2013). When ROS levels exceed the antioxidant capabilities of the cell, oxidative damage will ensue (Sheng et al, 2013).…”

Dietary potassium and cardiovascular profile. Results from the modification of diet in renal disease dataset

“…7 Moreover, reactive oxygen species are a critical mediator of the Na-K-ATPase pump signaling, and their generation can be attenuated by potassium transit into the cells. 8 Taking into consideration the type of the dataset analyzed and the cross-sectional nature of the analysis, our results cannot be expanded beyond a correlation, but when taken together with other existing evidence from animal and human experiments, it is reasonable to conclude that the protective effects of a high potassium diet can be explained by its antihypertensive and antioxidant properties. …”

Targeting Na/K-ATPase Signaling: A New Approach to Control Oxidative Stress

“…Increases in ROS and/or RNS (reactive nitrogen species) cause oxidative modification of the Na/K- ATPase α and β subunits along with FXYD proteins. S-glutathionylation, S-nitrosylation, and primary (direct) protein carbonylation are some of the many modifications which can be caused by oxidative stress [49–56]. These oxidative modifications may not only regulate (inhibit) the Na/K-ATPase enzymatic activity by blocking ouabain binding site, (thereby stabilizing the enzyme in E2 state due to conformational change), but may also promote the degradation of the enzyme.…”

“…1 ). Our proposed Na/K-ATPase signaling mediated oxidant amplification loop is based on our previous model [59], as well as 4 major observations described below [31, 32, 56–58, 60]. First, exogenous CTS stimulates Na/K-ATPase/c-Src signaling (and as a consequence, ROS generation), but in addition, Na/K-ATPase/c- src signaling is also stimulated by increases in ROS alone (caused by a) exogenously added H 2 O 2 , or b) exogenous, extracellular glu- cose oxidase, which produces H 2 O 2 at the expense of glucose in the culture medium).…”