유해활성산소 및 유해산화질소가 유발하는 핵과 소포체의 변화 분석

Analysis for Nucleus and Endoplasmic Reticulum Changes by Reactive Oxygen Species and Nitric Oxide

To investigate cross-talk between endoplasmic reticulum(ER) stress and oxidative stress in astroglioma, the cells were treated with hydrogen peroxide, DETA-NONOate and thapsigargin to raise intracellular levels of oxidative stress and ER stress, respectively. Cell viability was decreased in a dose-dependent manner in hydrogen peroxide- and DETA-NONOate - treated cells. Hydrogen peroxide, DETA-NONOate and thapsigargin also induced DNA fragmentation in these cells as indicated by terminal deoxynucleotidyl transferase-med iated dUTP nick end labeling. Hydrogen peroxide, DETA-NONOate and thapsigargin induced intracellular Ca2+ increase and perturbed Ca2+ homeostasis in endoplasmic reticulum(ER). Likewise, hydrogen peroxide, DETA-NONOate and thapsigargin also increased the expressions of ER stress- related molecules, IREl-a. The increase of IRE1 -a expression is coincided with those of p-JNK up on the treatment with hydrogen peroxide, DETA-NONOate, and thapsigargin in cells. These finding indicate that the increase of expression of IREl-a activating JNK pathway is induced during hydrogen peroxide, DETA-NONOate and thapsigargin - mediated cell death. Therefore, we conclude that oxidative stress including reactive oxygen species and nitric oxide cause nucleus and endoplasmic reticulum(ER) dysfunction and ER-related signals to occur in human astroglioma cells.