Anthracycline-containing chemotherapy causes long-term impairment of mitochondrial respiration and increased reactive oxygen species release in skeletal muscle
0301 basic medicine
0303 health sciences
Cell Respiration
Mitophagy
Antineoplastic Agents
DNA, Mitochondrial
Article
Dexamethasone
Mitochondria, Muscle
3. Good health
Mice
Oxidative Stress
03 medical and health sciences
Doxorubicin
Mutation
Animals
Anthracyclines
Female
Muscle, Skeletal
Reactive Oxygen Species
Sequence Deletion
DOI:
10.1038/srep08717
Publication Date:
2015-03-03T10:47:15Z
AUTHORS (15)
ABSTRACT
Abstract Anticancer treatments for childhood acute lymphoblastic leukaemia (ALL) are highly effective but now implicated in causing impaired muscle function long-term survivors. However, no comprehensive assessment of skeletal mitochondrial functions survivors has been performed and the presence persistent chemotherapy-induced dysfunction remains a strong possibility. Non-tumour-bearing mice were treated with two drugs that have used frequently ALL treatment (doxorubicin dexamethasone) up to 4 cycles at 3-week intervals euthanized 3 months after 4th cycle. Treated animals had growth lower mass as well reduced respiration increased reactive oxygen species production per unit consumption. Mitochondrial DNA content protein levels key membrane proteins markers biogenesis unchanged, Parkin reduced. This suggests novel pattern persists because an acquired defect mitophagy signaling. The results could explain observed functional impairments adult may also be relevant other cancers similar regimes.
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