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July 1, 2005Molecular Cancer Therapeutics

Manganese superoxide dismutase and inducible nitric oxide synthase modify early oxidative events in acute Adriamycin-induced mitochondrial toxicity

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Key result

Overexpression of MnSOD protected against acute Adriamycin-induced mitochondrial injury, whereas iNOS deficiency potentiated it compared with nontransgenic mice.

Why the study?

Does overexpression of MnSOD or knockout of iNOS modify acute Adriamycin-induced mitochondrial toxicity in mice?

Population

Genetically engineered B6C3 mice (overexpressing manganese superoxide dismutase [TgM], inducible nitric…

Comparison

Adriamycin 20 mg/kg vs Nontransgenic mice treated with Adriamycin

Design

Preclinical

Follow-up

24 hours

Authors

LCLuksana ChaiswingUniversity of Wisconsin–MadisonMCMarsha P. ColeUniversity of LouisvilleWIWanida IttaratMahidol University

Discussion

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Implication

Hypothesis-generating for MnSOD/iNOS modulation in anthracycline mitochondrial toxicity; human validation required before any clinical consideration.

Structured PICO

Does overexpression of MnSOD or knockout of iNOS modify acute Adriamycin-induced mitochondrial toxicity in mice?

P
Population
Genetically engineered B6C3 mice and nontransgenic mice treated with 20 mg/kg Adriamycin and evaluated up to 24 hours to study cardiotoxicity.
I
Intervention
Adriamycin 20 mg/kg
C
Comparator
Nontransgenic mice treated with Adriamycin
O
Outcome
Ultrastructural damage and levels of 4-hydroxy-2-nonenal (4HNE) protein adducts and 3-nitrotyrosine (3NT) in cardiomyocytes at 0, 3, 6, and 24 hourssurrogate

Overexpression of MnSOD protects against, while iNOS deficiency exacerbates, acute Adriamycin-induced mitochondrial injury in a murine model.

Cite This Study

Chaiswing et al. (2005) studied Acute Adriamycin-induced cardiotoxicity. MnSOD overexpression and iNOS deficiency vs. Nontransgenic mice was evaluated on Mitochondrial injury, 4HNE protein adducts, and 3NT levels. Overexpression of MnSOD protected against acute Adriamycin-induced mitochondrial injury, whereas iNOS deficiency potentiated it compared with nontransgenic mice.

synapsesocial.com/papers/6a9eb874db61d4274d478bc0https://doi.org/10.1158/1535-7163.mct-04-0322
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Intracellular distribution of peroxynitrite during doxorubicin cardiomyopathy: evidence for selective impairment of myofibrillar creatine kinase2002 · 114 citations
  2. 2Endothelial Nitric Oxide Synthase-Dependent Superoxide Generation from Adriamycin1997 · 371 citations
  3. 3Human Mn-superoxide dismutase in pulmonary epithelial cells of transgenic mice confers protection from oxygen injury.1992 · 315 citations
  4. 4The protective role of manganese superoxide dismutase against adriamycin-induced acute cardiac toxicity in transgenic mice.1996 · 461 citations