Mitochondrial thioredoxin in regulation of oxidant-induced cell death

Yan Chen; Jiyang Cai; Dean P. Jones

doi:10.1016/j.febslet.2006.11.007

Mitochondrial thioredoxin in regulation of oxidant-induced cell death

Yan Chen
, Jiyang Cai
, Dean P. Jones

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

87 Scopus citations

Abstract

Mitochondrial thioredoxin (mtTrx) can be oxidized in response to inducers of oxidative stress; yet the functional consequences of the oxidation have not been determined. This study evaluated the redox status of mtTrx and its association to oxidant-induced apoptosis. Results showed that mtTrx was oxidized after exposure to peroxides and diamide. Overexpression of mtTrx protected against diamide-induced oxidation and cytotoxicity. Oxidation of mtTrx was also achieved by knocking down its reductase; and lead to increased susceptibility to cell death. The data indicate that the redox status of mtTrx is a regulatory mechanism underlying the vulnerability of mitochondria to oxidative injury.

Original language	English (US)
Pages (from-to)	6596-6602
Number of pages	7
Journal	FEBS Letters
Volume	580
Issue number	28-29
DOIs	https://doi.org/10.1016/j.febslet.2006.11.007
State	Published - Dec 11 2006
Externally published	Yes

Keywords

Mitochondria
Oxidative stress
Redox
Thioredoxin
Thioredoxin reductase

ASJC Scopus subject areas

Structural Biology
Biophysics
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2006.11.007

Cite this

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title = "Mitochondrial thioredoxin in regulation of oxidant-induced cell death",

abstract = "Mitochondrial thioredoxin (mtTrx) can be oxidized in response to inducers of oxidative stress; yet the functional consequences of the oxidation have not been determined. This study evaluated the redox status of mtTrx and its association to oxidant-induced apoptosis. Results showed that mtTrx was oxidized after exposure to peroxides and diamide. Overexpression of mtTrx protected against diamide-induced oxidation and cytotoxicity. Oxidation of mtTrx was also achieved by knocking down its reductase; and lead to increased susceptibility to cell death. The data indicate that the redox status of mtTrx is a regulatory mechanism underlying the vulnerability of mitochondria to oxidative injury.",

keywords = "Mitochondria, Oxidative stress, Redox, Thioredoxin, Thioredoxin reductase",

author = "Yan Chen and Jiyang Cai and Jones, \{Dean P.\}",

note = "Funding Information: This research was supported by Grants from the NIH (ES09047, EY07892, ES014668); Carl M. Reeves and Mildred A. Reeves Foundation; International Retinal Research Foundation, Inc.; a departmental Challenge Grant and Sybil Harrington Award (to JC) from Research to Prevent Blindness, Inc.",

year = "2006",

month = dec,

day = "11",

doi = "10.1016/j.febslet.2006.11.007",

language = "English (US)",

volume = "580",

pages = "6596--6602",

journal = "FEBS Letters",

issn = "0014-5793",

publisher = "John Wiley and Sons Inc.",

number = "28-29",

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TY - JOUR

T1 - Mitochondrial thioredoxin in regulation of oxidant-induced cell death

AU - Chen, Yan

AU - Cai, Jiyang

AU - Jones, Dean P.

N1 - Funding Information: This research was supported by Grants from the NIH (ES09047, EY07892, ES014668); Carl M. Reeves and Mildred A. Reeves Foundation; International Retinal Research Foundation, Inc.; a departmental Challenge Grant and Sybil Harrington Award (to JC) from Research to Prevent Blindness, Inc.

PY - 2006/12/11

Y1 - 2006/12/11

N2 - Mitochondrial thioredoxin (mtTrx) can be oxidized in response to inducers of oxidative stress; yet the functional consequences of the oxidation have not been determined. This study evaluated the redox status of mtTrx and its association to oxidant-induced apoptosis. Results showed that mtTrx was oxidized after exposure to peroxides and diamide. Overexpression of mtTrx protected against diamide-induced oxidation and cytotoxicity. Oxidation of mtTrx was also achieved by knocking down its reductase; and lead to increased susceptibility to cell death. The data indicate that the redox status of mtTrx is a regulatory mechanism underlying the vulnerability of mitochondria to oxidative injury.

AB - Mitochondrial thioredoxin (mtTrx) can be oxidized in response to inducers of oxidative stress; yet the functional consequences of the oxidation have not been determined. This study evaluated the redox status of mtTrx and its association to oxidant-induced apoptosis. Results showed that mtTrx was oxidized after exposure to peroxides and diamide. Overexpression of mtTrx protected against diamide-induced oxidation and cytotoxicity. Oxidation of mtTrx was also achieved by knocking down its reductase; and lead to increased susceptibility to cell death. The data indicate that the redox status of mtTrx is a regulatory mechanism underlying the vulnerability of mitochondria to oxidative injury.

KW - Mitochondria

KW - Oxidative stress

KW - Redox

KW - Thioredoxin

KW - Thioredoxin reductase

UR - https://www.scopus.com/pages/publications/33751509841

UR - https://www.scopus.com/pages/publications/33751509841#tab=citedBy

U2 - 10.1016/j.febslet.2006.11.007

DO - 10.1016/j.febslet.2006.11.007

M3 - Article

C2 - 17113580

AN - SCOPUS:33751509841

SN - 0014-5793

VL - 580

SP - 6596

EP - 6602

JO - FEBS Letters

JF - FEBS Letters

IS - 28-29

ER -

Mitochondrial thioredoxin in regulation of oxidant-induced cell death

Abstract

Keywords

ASJC Scopus subject areas

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