Gp91phox-containing NAD(P)H oxidase increases superoxide formation by doxorubicin and NADPH

Deng, Shiwei; Krüger, Anke; Kleschyov, Andrei L.; Kalinowski, Leszek; Daiber, Andreas; Wojnowski, Leszek

doi:10.1016/j.freeradbiomed.2006.11.013

Cited by 86 publications

(72 citation statements)

References 47 publications

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“…Moreover, the results obtained in our animal model are also in line with the active implication of NADPH oxidases in the apoptotic death induced by doxorubicin to cardiomyocytes in vitro reported by Gilleron et al, (2009). Nox2 and Nox4 are the major isoforms of Nox expressed in cardiac tissue (Santos et al 2011), but previous works have pointed out that Nox2 is the isoform activated in doxorubicin cardiotoxicity (Deng et al 2007;Yoshida et al 2009;Huelsenbeck et al 2011) as well as in cardiac hypertrophy (Santos et al, 2011;Takemoto et al, 2001). Our results exclude up-regulation of the expression of the main Nox2 subunits gp91phox and p22phox, but it is to be noted that recruitment of cytosolic subunits of Nox2 expressed in heart tissue can lead to the observed activation of this enzyme by doxorubicin treatment, as pointed out by Yoshida et al, 2009 and Huelsenbeck et al, 2011.…”

Section: Discussionmentioning

confidence: 99%

“…Since Deng et al, (2007) have pointed to Nox2, composed of the catalytic subunit gp91phox and the membrane binding partner p22phox, as the most probable isoform activated in the cardiotoxic process, we have performed Western blotting analysis of the heart homogenates using antigp91phox (cat. number 611415 from BD Transduction Laboratories, Lexington, KY, USA) and anti-p22phox (cat.…”

Section: C Of Supplementary Data)mentioning

confidence: 99%

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The decrease of NAD(P)H:quinone oxidoreductase 1 activity and increase of ROS production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity

Lagoa

Gañan²,

López‐Sánchez³

et al. 2014

Biomarkers

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Context. Doxorubicin cardiotoxicity displays a complex and multifactorial progression.Objective. Identify early biochemical mechanisms leading to a sustained imbalance of cellular bioenergetics.Methods. Measurements of the temporal evolution of selected biochemical markers after treatment of rats with doxorubicin (20 mg/kg body weight).Results. Doxorubicin treatment increased lipid oxidation, catalase activity and production of H2O2 by Nox-NADPH oxidases, and down-regulated NAD(P)H:quinone oxidoreductase-1 prior eliciting changes in reduced glutathione, protein carbonyls and protein nitrotyrosines. Alterations of mitochondrial and myofibrillar bioenergetics biomarkers were detected only after this oxidative imbalance was established.Conclusions. NAD(P)H:quinone oxidoreductase-1 activity and increase of hydrogen peroxide production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity.

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Section: Discussionmentioning

confidence: 99%

Section: C Of Supplementary Data)mentioning

confidence: 99%

The decrease of NAD(P)H:quinone oxidoreductase 1 activity and increase of ROS production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity

Lagoa

Gañan²,

López‐Sánchez³

et al. 2014

Biomarkers

View full text Add to dashboard Cite

show abstract

“…Maytin et al have indicated that myocardial hypertrophy induced by chronic pressure overload after aortic constriction was also not affected in gp91 phox knockout mice (43). However, another study has shown the reduced cardiotoxicity following doxorubicin treatment in gp91 phox knockout mice (44). Taking together, these studies suggest that gp91 phox has different functions in cardiac remodeling depending on the nature of cardiac damage.…”

Section: Discussionmentioning

confidence: 99%

Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase

Zhao¹,

Zhao²,

Yan³

et al. 2009

Cardiovascular Pathology

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Background-There is growing recognition that oxidative stress plays a role in the pathogeneses of myocardial repair/remodeling following infarction (MI). NADPH oxidase is a major source for cardiac reactive oxygen species production. Herein, we studied the importance of NADPH oxidase in development of cardiac oxidative stress and its induced molecular and cellular changes related to myocardial repair/remodeling.

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“…As a model system we used doxorubicin (dox), a potent inducer of superoxide in cardiomyocytes (10). The production of superoxide by dox is catalyzed by NADPH oxidase (Nox) enzymes, which are important mediators of dox cardiotoxicity in vivo (11).…”

Section: Snornasmentioning

confidence: 99%

Cytosolic Accumulation of Small Nucleolar RNAs (snoRNAs) Is Dynamically Regulated by NADPH Oxidase

Holley¹,

Li²,

Scruggs³

et al. 2015

Journal of Biological Chemistry

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Background: Small nucleolar RNAs (snoRNAs) are thought to be exclusively nuclear. Results: Doxorubicin stress results in significant accumulation of cytosolic snoRNAs via a pathway involving Nox4D and superoxide. Conclusion: snoRNAs are present in the cytoplasm, and their cytosolic abundance is dynamically regulated. Significance: Previously unexplained snoRNA biology may be the result of snoRNA interactions with cytoplasmic targets.

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Gp91phox-containing NAD(P)H oxidase increases superoxide formation by doxorubicin and NADPH

Cited by 86 publications

References 47 publications

The decrease of NAD(P)H:quinone oxidoreductase 1 activity and increase of ROS production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity

The decrease of NAD(P)H:quinone oxidoreductase 1 activity and increase of ROS production by NADPH oxidases are early biomarkers in doxorubicin cardiotoxicity

Cardiac oxidative stress and remodeling following infarction: role of NADPH oxidase

Cytosolic Accumulation of Small Nucleolar RNAs (snoRNAs) Is Dynamically Regulated by NADPH Oxidase

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