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• W2016838845 abstract "Previous studies have shown that metallothionein (MT) can antagonize the myocardiotoxicity induced by doxorubicin (Dox), a most effective anticancer agent. However, the molecular mechanisms are not well-understood. Using a proteomics approach we have detected that major peroxiredoxins (Prxs), an important redox regulating molecule family, may be involved in this process. In the present study, we assessed a link between metallothionein and peroxiredoxins. Wild-type (MT(+/+)) and MT(-/-) mice were treated intraperitoneally with doxorubicin at a single dose of 15 mg/kg and sacrificed on the 4th day after treatment. Doxorubicin induced cardiotoxicity in both wild-type and MT(-/-) mice was manifested with increased serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities, and cardiac morphological changes. These toxic responses were stronger in the hearts of MT(-/-) mice that were more vulnerable to doxorubicin-induced oxidative injury as exhibited by increased lipid peroxidation and decreased catalase and glutathione peroxidase (GSH-Px) expression. Moreover, in the MT(-/-) mice, the deficiency of metallothionein inhibited the expression of Cu/Zn Superoxide dismutase (SOD-1) induced by doxorubicin. Doxorubicin significantly increased the mRNA levels and protein expressions of Prx-1, -2, -3, -5, and -6 in the hearts of wild-type but not MT(-/-) mice. Therefore, the present study suggests that metallothionein provides protection against doxorubicin-induced cardiotoxicity, which possibly involves regulation of peroxiredoxins." @default.
• W2016838845 created "2016-06-24" @default.
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• W2016838845 date "2011-06-01" @default.
• W2016838845 modified "2023-09-26" @default.
• W2016838845 title "Peroxiredoxins are involved in metallothionein protection from doxorubicin cardiotoxicity" @default.
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• W2016838845 doi "https://doi.org/10.1016/j.ejphar.2011.03.031" @default.
• W2016838845 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21463615" @default.
• W2016838845 hasPublicationYear "2011" @default.
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