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

76 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

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2006.11.007

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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",

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

language = "English (US)",

volume = "580",

pages = "6596--6602",

journal = "FEBS Letters",

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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

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IS - 28-29

ER -

Mitochondrial thioredoxin in regulation of oxidant-induced cell death

Abstract

Keywords

ASJC Scopus subject areas

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