Key result
Fullerenol/doxorubicin nanocomposite significantly reduced doxorubicin-induced oxidative stress (catalase mRNA, p<0.05) and increased antiapoptotic Bcl-2 mRNA (p<0.05) in rat myocardial tissue.
Why the study?
Does fullerenol/doxorubicin nanocomposite reduce acute cardiotoxic effects compared to doxorubicin alone in Wistar rats?
Does fullerenol/doxorubicin nanocomposite reduce acute cardiotoxic effects compared to doxorubicin alone in Wistar rats?
Fullerenol/doxorubicin nanocomposite mitigates doxorubicin-induced acute oxidative stress and apoptosis in rat myocardial tissue, suggesting a potential strategy to reduce anthracycline cardiotoxicity.
Answers are grounded in this paper and cite their sources.
Mitigates doxorubicin cardiotoxicity markers in rats; hypothesis-generating for human cardioprotection, needs prospective trials.
) is present in aqueous solutions in the form of polyanion nanoparticles with particles' size distribution within the range from 15 to 42 nm. In this research it is assumed that these features could enable fullerenol nanoparticles (FNPs) to bind positively charged molecules like doxorubicin (DOX) and serve as drug carriers. Considering this, fullerenol/doxorubicin nanocomposite (FNP/DOX) is formed and characterized by ultra-performance liquid chromatography tandem mass spectrometry, dynamic light scattering, atomic force microscopy and transmission electron microscopy. Measurements have shown that DOX did not significantly affect particle size (23 nm). It is also assumed that FNP/DOX could reduce the acute cardiotoxic effects of DOX in vivo (Wistar rats treated i.p.). In this study, quantitative real time polymerase chain reaction results have shown that treatment with DOX alone caused significant increase in mRNA levels of catalase (p < 0.05) enzyme indicating the presence of oxidative stress. This effect is significantly reduced by the treatment with FNP/DOX (p < 0.05). Furthermore, mRNA levels of antiapoptotic enzyme (Bcl-2) are significantly increased (p < 0.05) in all treated groups, particularly where FNP/DOX was applied, suggesting cell resistance to apoptosis. Moreover, ultrastructural analysis has shown the absence of myelin figures within the mitochondria in the heart tissue with FNP/DOX treatment, indicating reduction of oxidative stress. Hence, our results have implied that FNP/DOX is generally less harmful to the heart compared to DOX.
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Seke et al. (2016) studied Doxorubicin-induced acute cardiotoxicity. Fullerenol/doxorubicin nanocomposite (FNP/DOX) vs. Doxorubicin (DOX) alone was evaluated on mRNA levels of catalase and Bcl-2 (p=<0.05). Fullerenol/doxorubicin nanocomposite significantly reduced doxorubicin-induced oxidative stress (catalase mRNA, p<0.05) and increased antiapoptotic Bcl-2 mRNA (p<0.05) in rat myocardial tissue.
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