Role of reactive oxygen species (ROS) in apoptosis induction

H. U. Simon; A. Haj-Yehia; F. Levi-Schaffer

doi:10.1023/A:1009616228304

Role of reactive oxygen species (ROS) in apoptosis induction

H. U. Simon^*
, A. Haj-Yehia
, F. Levi-Schaffer

^*Corresponding author for this work

School of Pharmacy

Research output: Contribution to journal › Article › peer-review

2664 Scopus citations

Abstract

Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.

Original language	English
Pages (from-to)	415-418
Number of pages	4
Journal	Apoptosis
Volume	5
Issue number	5
DOIs	https://doi.org/10.1023/A:1009616228304
State	Published - 2000

Bibliographical note

Funding Information:
Work of the laboratory of H.U.S. is supported by the Swiss National Science Foundation (31-58916.99), the EMDO Foundation Zurich. Foundation Novartis Basel Helmut Horten Foundation Madonna del Piano, and Stiftung Zur Krebsbekämpting Zürich.

Keywords

Apoptosis
Death receptors
Inflammation
Reactive oxygen species (ROS)

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10.1023/A:1009616228304

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title = "Role of reactive oxygen species (ROS) in apoptosis induction",

abstract = "Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.",

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note = "Funding Information: Work of the laboratory of H.U.S. is supported by the Swiss National Science Foundation (31-58916.99), the EMDO Foundation Zurich. Foundation Novartis Basel Helmut Horten Foundation Madonna del Piano, and Stiftung Zur Krebsbek{\"a}mpting Z{\"u}rich.",

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AU - Simon, H. U.

AU - Haj-Yehia, A.

AU - Levi-Schaffer, F.

N1 - Funding Information: Work of the laboratory of H.U.S. is supported by the Swiss National Science Foundation (31-58916.99), the EMDO Foundation Zurich. Foundation Novartis Basel Helmut Horten Foundation Madonna del Piano, and Stiftung Zur Krebsbekämpting Zürich.

PY - 2000

Y1 - 2000

N2 - Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.

AB - Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.

KW - Apoptosis

KW - Death receptors

KW - Inflammation

KW - Reactive oxygen species (ROS)

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ER -

Role of reactive oxygen species (ROS) in apoptosis induction

Abstract

Bibliographical note

Keywords

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