超氧化物
活性氧
SOD2
线粒体
超氧化物歧化酶
过氧化氢酶
线粒体ROS
氧化磷酸化
SOD1
化学
生物化学
线粒体内膜
氧化应激
生物
细胞生物学
酶
作者
Jan M. Suski,Magdalena Lebiedzińska,Massimo Bonora,Paolo Pinton,Jerzy Duszyński,Mariusz R. Wiȩckowski
出处
期刊:Methods in molecular biology
日期:2018-01-01
卷期号:: 357-381
被引量:90
标识
DOI:10.1007/978-1-4939-7831-1_22
摘要
Mitochondria are considered the main source of reactive oxygen species (ROS) in the cell. For this reason they have been recognized as a source of various pathological conditions as well as aging. Chronic increase in the rate of ROS production is responsible for the accumulation of ROS-associated damages in DNA, proteins, and lipids and may result in progressive cell dysfunctions and, in a consequence, apoptosis, increasing the overall probability of an organism's pathological conditions. The superoxide anion is the main undesired by-product of mitochondrial oxidative phosphorylation. Its production is triggered by a leak of electrons from the mitochondrial respiratory chain and the reaction of these electrons with O2. Superoxide dismutase (MnSOD, SOD2) from the mitochondrial matrix, as well as superoxide dismutase (Cu/ZnSOD, SOD1) present in small amounts in the mitochondrial intramembrane space, converts superoxide anion to hydrogen peroxide, which can be then converted by catalase to harmless H2O.In the chapter we describe a relation between mitochondrial membrane potential and the rate of ROS formation. We present different methods applicable for isolated mitochondria or intact cells. We also present experiments demonstrating that a magnitude and a direction (increase or decrease) of a change in mitochondrial ROS production depend on the metabolic state of this organelle.
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