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Angaben zur Quelle [Bearbeiten]

Autor     Shazib Pervaiz, Marie-Veronique Clement
Titel    Superoxide anion: Oncogenic reactive oxygen species?
Zeitschrift    The International Journal of Biochemistry & Cell Biology
Verlag    Elsevier
Ausgabe    39
Jahr    2007
Seiten    1297–1304
URL    http://www.sciencedirect.com/science/article/pii/S1357272507001240

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Fragmente    1


Fragmente der Quelle:
[1.] Src/Fragment 026 15 - Diskussion
Zuletzt bearbeitet: 2014-09-27 20:22:26 Kybot
Fragment, Pervaiz and Clement 2007, SMWFragment, Schutzlevel, Src, Verschleierung, ZuSichten

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Untersuchte Arbeit:
Seite: 26, Zeilen: 15-29
Quelle: Pervaiz and Clement 2007
Seite(n): 1297, 1298, Zeilen: 1297: l. Spalte: 4ff; 1298: r. Spalte: 13ff
The major reactive oxygen species (ROS) include oxygen radicals such as superoxide (O2−) and hydroxyl (OH), as well as non-radical derivatives of molecular oxygen (O2), such as hydrogen peroxide (H2O2). Whereas O2− and H2O2 do not exhibit strong reactivity with other bio-molecules, their reaction generates the highly reactive OH radical, which probably accounts for most of the oxidative damage attributed to ROS (Halliwell & Gutteridge, 1999).

In healthy living cells, one or more of redox regulatory mechanisms are activated in response to a transient increase in intracellular ROS to prevent oxidative stress. A disturbance in the tight balance between ROS production and elimination, either via augmentation of ROS generation or defective/deficient anti-oxidant defenses for their elimination, results in a build up of intracellular ROS and may lead to persistent changes in signal transduction and gene expression (Sauer et al., 2001), thereby giving rise to oxidative stress-related pathological states (Burdon, 1995 and Burdon, 1996).

Leaving aside the reactive nitrogen species, the major reactive oxygen species (ROS) include oxygen radicals such as superoxide (O2 −) and hydroxyl (•OH), as well as non-radical derivatives of molecular oxygen (O2), such as hydrogen peroxide (H2O2) (Fridovich, 1978). Whereas O2 − and H2O2 do not exhibit strong reactivity with other bio-molecules, their reaction generates the highly reactive •OH radical, which probably accounts for most of the oxidative damage attributed to ROS (Halliwell & Gutteridge, 1999).

[Seite 1298]

In healthy living cells, one or more of these redox regulatory mechanisms are activated in response to a transient increase in intracellular ROS to prevent oxidative stress. A disturbance in the tight balance between ROS production and elimination, either via augmentation of ROS generation or defective/deficient anti-oxidant defenses for their elimination, results in a build up of intracellular ROS and may lead to persistent changes in signal transduction and gene expression, thereby giving rise to oxidative stress-related pathological states.

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