Doxorubicin-induced persistent oxidative stress to cardiac myocytes. (Q43615200)

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7 November 2019

title

Doxorubicin-induced persistent oxidative stress to cardiac myocytes (English)

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7 November 2019

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7 November 2019

S Zhou

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7 November 2019

K B Wallace

series ordinal

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7 November 2019

publication date

1 May 2001

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7 November 2019

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7 November 2019

volume

121

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7 November 2019

issue

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7 November 2019

page(s)

151-157

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Reduced mitochondrial DNA transcription in senescent rat heart

7 November 2019

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Role of xanthine oxidase in the potentiation of doxorubicin-induced cardiotoxicity by mitomycin C

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Molecular mechanisms of doxorubicin-induced cardiomyopathy. Selective suppression of Reiske iron-sulfur protein, ADP/ATP translocase, and phosphofructokinase genes is associated with ATP depletion in rat cardiomyocytes

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Ellman's reagent: 5,5′-dithiobis(2-nitrobenzoic acid)—a reexamination

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Preferential mitochondrial DNA injury caused by glucose oxidase as a steady generator of hydrogen peroxide in human fibroblasts

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Cardioselective and cumulative oxidation of mitochondrial DNA following subchronic doxorubicin administration 1Supported in part by NIH Grant HL58016. The manuscript was not subjected to internal Agency review and, thus, the opinions are those of the

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7 January 2021

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7 January 2021

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7 January 2021

Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria

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7 January 2021

Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress

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7 January 2021

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7 January 2021

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Identifiers

DOI

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7 November 2019

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