Key result
Treatment of H9c2 cardiomyocytes with 1 µM doxorubicin led to a transient increase in the nuclear level of poly(ADP-ribosyl)ated proteins after 6 hours of incubation.
Doxorubicin induces transient activation of protein poly(ADP-ribosyl)ation in H9c2 cardiomyocytes, suggesting the development of genotoxic stress.
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Suggests early genotoxic stress marker in doxorubicin-exposed cardiomyocytes; hypothesis-generating and leaves open clinical relevance.
Possible involvement of the system of protein poly(ADP-ribosyl)ation in the mechanisms of cardiotoxicity of doxorubicin, one of the most frequently used anticancer drug, was studied in cultures of cardiomyocytes H9c2. The treatment of H9c2 cells with doxorubicin (1 µM) led to a transient (after 6 h of incubation) increase in the nuclear level of poly(ADP-ribosyl)ated proteins. The observed data indirectly indicate the development of genotoxic stress in the doxorubicin-treated cells, probably caused by the stimulatory effects of doxorubicin and its metabolites on the production of reactive oxygen and nitrogen species.
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Efremovа et al. (2015) studied Doxorubicin cardiotoxicity. Doxorubicin was evaluated on Nuclear level of poly(ADP-ribosyl)ated proteins. Treatment of H9c2 cardiomyocytes with 1 µM doxorubicin led to a transient increase in the nuclear level of poly(ADP-ribosyl)ated proteins after 6 hours of incubation.
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