[Mitochondrial dysfunction as a promoting factor of senescence].
Masamichi Ikawa, Makoto Yoneda
Abstract
Masamichi Ikawa, Makoto Yoneda
Abstract
Mitochondria not only produce the cell's ATP using oxygen, but also act as a major source of reactive oxygen species (ROS). ROS are generated as by-products in normal oxidative metabolism, and are eliminated by antioxidants in ordinary circumstances. Mitochondrial dysfunction induces the increase of ROS generation, and excess ROS injure the genes, proteins and lipids in mitochondria and cells (oxidative stress). Particularly, oxidative damages to mitochondrial DNA provoke further mitochondrial respiratory chain damage and oxidative stress. Oxidative damages in mitochondria and cells are increased during aging, therefore mitochondrial dysfunction and oxidative stress play crucial roles in promoting senescence. Mitochondria are important targets for anti-aging.
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Mitochondria not only produce the cell's ATP using oxygen, but also act as a major source of reactive oxygen species (ROS). ROS are generated as by-products in normal oxidative metabolism, and are eliminated by antioxidants in ordinary circumstances. Mitochondrial dysfunction induces the increase of ROS generation, and excess ROS injure the genes, proteins and lipids in mitochondria and cells (oxidative stress). Particularly, oxidative damages to mitochondrial DNA provoke further mitochondrial respiratory chain damage and oxidative stress. Oxidative damages in mitochondria and cells are increased during aging, therefore mitochondrial dysfunction and oxidative stress play crucial roles in promoting senescence. Mitochondria are important targets for anti-aging.
Key concepts: Oxidative stress, Mitochondrion, Reactive oxygen species, Senescence, Oxidative phosphorylation, Mitochondrial ROS, Mitochondrial DNA, Cell biology