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    Sodium nitrate co-supplementation does not exacerbate low dose metronomic doxorubicin-induced cachexia in healthy mice

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    Author
    Campelj, DG; Debruin, DA; Timpani, CA; Hayes, A; Goodman, CA; Rybalka, E
    Date
    2020-09-24
    Source Title
    Scientific Reports
    Publisher
    NATURE RESEARCH
    University of Melbourne Author/s
    Goodman, Craig; Hayes, Alan
    Affiliation
    Physiology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Campelj, D. G., Debruin, D. A., Timpani, C. A., Hayes, A., Goodman, C. A. & Rybalka, E. (2020). Sodium nitrate co-supplementation does not exacerbate low dose metronomic doxorubicin-induced cachexia in healthy mice. SCIENTIFIC REPORTS, 10 (1), https://doi.org/10.1038/s41598-020-71974-z.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251633
    DOI
    10.1038/s41598-020-71974-z
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7518269
    Abstract
    The purpose of this study was to determine whether (1) sodium nitrate (SN) treatment progressed or alleviated doxorubicin (DOX)-induced cachexia and muscle wasting; and (2) if a more-clinically relevant low-dose metronomic (LDM) DOX treatment regimen compared to the high dosage bolus commonly used in animal research, was sufficient to induce cachexia in mice. Six-week old male Balb/C mice (n = 16) were treated with three intraperitoneal injections of either vehicle (0.9% NaCl; VEH) or DOX (4 mg/kg) over one week. To test the hypothesis that sodium nitrate treatment could protect against DOX-induced symptomology, a group of mice (n = 8) were treated with 1 mM NaNO3 in drinking water during DOX (4 mg/kg) treatment (DOX + SN). Body composition indices were assessed using echoMRI scanning, whilst physical and metabolic activity were assessed via indirect calorimetry, before and after the treatment regimen. Skeletal and cardiac muscles were excised to investigate histological and molecular parameters. LDM DOX treatment induced cachexia with significant impacts on both body and lean mass, and fatigue/malaise (i.e. it reduced voluntary wheel running and energy expenditure) that was associated with oxidative/nitrostative stress sufficient to induce the molecular cytotoxic stress regulator, nuclear factor erythroid-2-related factor 2 (NRF-2). SN co-treatment afforded no therapeutic potential, nor did it promote the wasting of lean tissue. Our data re-affirm a cardioprotective effect for SN against DOX-induced collagen deposition. In our mouse model, SN protected against LDM DOX-induced cardiac fibrosis but had no effect on cachexia at the conclusion of the regimen.

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