Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc.

@article{Arany2013ChronicNE,
  title={Chronic nicotine exposure augments renal oxidative stress and injury through transcriptional activation of p66shc.},
  author={Istvan Arany and Jeb S. Clark and Dustin K. Reed and Luis A Juncos},
  journal={Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association},
  year={2013},
  volume={28 6},
  pages={1417-25}
}
BACKGROUND Chronic nicotine (Ch-NIC) exposure exacerbates ischemia/reperfusion (I/R)-induced oxidative stress and acute kidney injury (AKI), and mitochondrial production of reactive oxygen species (ROS) in cultured renal proximal tubule cells (RPTCs). Because Ser36-phosphorylated p66shc modulates mitochondrial ROS production and injury of RPTCs, we hypothesized that Ch-NIC exacerbates AKI by increasing stress-induced phosphorylation of p66shc. METHODS We first tested whether Ch-NIC augments I… CONTINUE READING
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