著者
富田 和男 桑原 義和 高 裕子 並河 英紀 西谷 佳浩 漆原 佑介 山西 沙祐里 古川 みなみ 宮脇 正一 栗政 明弘 福本 学 佐藤 友昭
出版者
東北医科薬科大学
雑誌
東北医科薬科大学研究誌 = Journal of Tohoku Medical and Pharmaceutical University (ISSN:24325724)
巻号頁・発行日
no.64, pp.49-55, 2017

Oxidative stress is a harmful state for the cell. The state arises from exposure to high levels of reactive oxygen species(ROS).ROS is a key molecule in maintaining cell proliferation, inflammation and cell death. ROS is also involved in aging and causes many diseases such as Parkinson s disease, Alzheimer s disease, cancer, diabetes mellitus and periodontal disease. The primary site of ROS generation in vivo is mitochondria. Mitochondria have its own DNA(mtDNA)that encodes a part of oxidative phosphorylation component proteins in mitochondria, and mtDNA damage by ROS causes neurodegenerative diseases and various types of cancer. Therefore, these damaged cells will provide valuable cell models to study oxidative stress and overcome ROS derived diseases. To analyze the mechanism of oxidative stress and ROS derived diseases, mtDNA depleted cells(ρ0 cells)are developed by treating low dose ethidium bromide. ρ0 cells do not have mtDNA, can't survive without pyruvate and uridine, produce little amount of ATP, sensitive to oxidative stress and generate higher ROS compared with parental cell. in this review, we describe the cellular response by oxidative stress such as radiation and hydrogen peroxide using ρ0 cells. we also discuss the relationship among oxidative stress sensitivity, mitochondria damage and plasma membrane status.