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  1. KEEP
  2. Theses and Dissertations
  3. Barrett, The Honors College Thesis/Creative Project Collection
  4. Doxorubicin Induced Cardiotoxicity and High Intensity Aerobic Exercise
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Doxorubicin Induced Cardiotoxicity and High Intensity Aerobic Exercise

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Description

Doxorubicin (DOX) is a cardiotoxic, anthracycline-based, anti-neoplastic agent that causes pathological cardiac remodeling due to altered protein expression associated with cardiotoxicity. DOX cardiotoxicity causes increased Akt phosphorylation, blunted AMPK phosphorylation and upregulated mTOR phosphorylation. Akt is activated by cellular stress and damage. AMPK is activated by increases in AMP and ADP concentrations and decreased ATP concentration. mTOR is active in cellular growth and remodeling. These proteins are cellular kinases with cascades that are influenced by one another. Exercise preconditioning may diminish the cardiotoxic effects on these proteins. Female, Ovariectomized Sprague-Dawley rats (N=33) were randomized to: Exercise+DOX (EX+DOX, n=9); Exercise+Vehicle (EX+VEH, n=8); Sedentary+DOX (SED+DOX, n=8); and Sedentary+Vehicle (SED+VEH, n=8) groups. DOX (4mg/kg) or VEH (saline) intraperitoneal injections were administered bi-weekly (cumulative dose of 12mg/kg). VEH animals received body weight matched volumes of saline based on dosing in animals receiving DOX. Exercise (EX) animals underwent high intensity (85-95% VO2 peak) interval training (HIIT) (4x4 min bouts) separated by low intensity (50-60% VO2max) intervals (2 min bouts) 5 days per week. Exercise began 1 week prior to the first injection and was continued throughout the study. Rats were euthanized 5 days after the last injection. Left ventricular tissue was isolated, processed into lysate and used for western blot analyses [2x2 ANOVA; (α=0.05)]. DOX induced significant phosphorylation of Akt and mTOR (p=0.035; p=0.032) only in SED+DOX rats, but unchanged in EX+DOX rats. No significant differences (p=0.374) in AMPK phosphorylation were observed between groups. Exercise Preconditioning prevents some DOX-induced changes in the cardiac mTOR signaling pathway implicated in pathological remodeling.

Date Created
2017-05
Contributors
  • Panknin, Timothy M (Author)
  • Angadi, Siddhartha (Thesis director)
  • Sweazea, Karen (Committee member)
  • Dickinson, Jared (Committee member)
  • School of Nutrition and Health Promotion (Contributor)
  • Barrett, The Honors College (Contributor)
Topical Subject
  • cancer research
  • High-intensity Interval Training
  • Cardioprotection
  • Cardiotoxicity
  • Exercise
  • Cardiac
Resource Type
Text
Extent
26 pages
Language
eng
Copyright Statement
In Copyright
Primary Member of
Barrett, The Honors College Thesis/Creative Project Collection
Series
Academic Year 2016-2017
Handle
https://hdl.handle.net/2286/R.I.42906
Level of coding
minimal
Cataloging Standards
asu1
System Created
  • 2017-10-30 02:50:58
System Modified
  • 2021-08-11 04:09:57
  •     
  • 1 year 5 months ago
Additional Formats
  • OAI Dublin Core
  • MODS XML

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