These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: [Role of mitochondria in reactive oxygen species generation and removal; relevance to signaling and programmed cell death].
    Author: Czarna M, Jarmuszkiewicz W.
    Journal: Postepy Biochem; 2006; 52(2):145-56. PubMed ID: 17078504.
    Abstract:
    Reactive oxygen species (ROS) are universal products of aerobic metabolism, which can be also produced in stress conditions. In eukaryotic cells, mitochondria are the main source of ROS. The main mitochondrial sites of ROS formation are electron carriers of respiratory chain. However, there are also other enzymatic sites capable of ROS generation in different mitochondrial compartments. Reactive oxygen species can cause serious damage to many biological macromolecules, such as proteins, lipids and nucleic acids, which oxidation leads to a lost of their biological properties and eventually to a cell death. Mitochondria, which are also exposed to harmful ROS action, have a defense system that decreases ROS production (first line of defense) or removes generated ROS (second line of defense). Mitochondrial antioxidant system involves proteins that decrease ROS formation, enzymes that directly react with ROS, and non-enzymatic antioxidants that also remove ROS and other oxygen derivatives. Mitochondrial ROS can also act as signal messengers and modify operation of many routes in different cell compartments. Mitochondrial ROS are also important in execution of programmed cell death.
    [Abstract] [Full Text] [Related] [New Search]