Antioxidants protect against reactive oxygen species associated with adriamycin-treated cardiomyocytes.

  title={Antioxidants protect against reactive oxygen species associated with adriamycin-treated cardiomyocytes.},
  author={S M DeAtley and Michael Y. Aksenov and Marina V. Aksenova and Brianna Harris and R A Hadley and P Cole Harper and John M. Carney and David Allan Butterfield},
  journal={Cancer letters},
  volume={136 1},

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  • G. Oktem, A. Uysal, A. Bilir
  • Biology, Medicine
    Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie
  • 2012


Failure of the antioxidant vitamin E to protect against adriamycin-induced cardiotoxicity in the rabbit.
Vitamin E does not protect against the development of cardiomyopathy and contractile decline after chronic exposure to Adriamycin, andoadministration of vitamin E did result in an increased life span.
Enalaprilat inhibits hydrogen peroxide production by murine mesangial cells exposed to high glucose concentrations.
Enalaprilat has an antioxidant effect in cultured mesangial cells, not linked to ACE inhibition, but may be related to an inhibition of the PKC system.
Adriamycin induces protein oxidation in erythrocyte membranes.
Results are consistent with the notion that oxidative modification of membrane proteins may contribute to the development of the acute adriamycin-mediated toxicity.
The anti-oxidant properties of 5-aminosalicylic acid.
Oxidative and non-oxidative mechanisms in the inactivation of cardiac mitochondrial electron transport chain components by doxorubicin.
The results indicate that low concentrations of doxorubicin (50 microM or less) can catalyse a site-specific oxidative damage to the NADH oxidation pathway, and ten-fold higher doxorbicin concentrations are required for non-oxidative inactivation of the electron transport chain.
Effect of anthracycline antibiotics on oxygen radical formation in rat heart.
The results suggest that free radical formation by the anthracycline antitumor agents, which occurs in the same myocardial compartments that are subject to drug-induced tissue injury, may damage the heart by exceeding the oxygen radical detoxifying capacity of cardiac mitochondria and sarcoplasmic reticulum.
Probucol protects against adriamycin cardiomyopathy without interfering with its antitumor effect.
These data show for the first time that PROB can provide complete protection against ADR cardiomyopathy without interfering with antitumor properties of the drug.
The spin trap alpha-phenyl-tert-butyl nitrone protects against myelotoxicity and cardiotoxicity of adriamycin while preserving the cytotoxic activity.
The present results suggest that a proper administration schedule of spin traps might be a promising approach for improving the therapeutic index of ADR.
Analyses of the molecular mechanism of adriamycin-induced cardiotoxicity.