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Astaxanthin but not quercetin preserves mitochondrial integrity and function, ameliorates oxidative stress, and reduces heat-induced skeletal muscle injury.

Publication ,  Journal Article
Yu, T; Dohl, J; Chen, Y; Gasier, HG; Deuster, PA
Published in: J Cell Physiol
August 2019

Heat stress causes mitochondrial dysfunction and increases mitochondrial production of reactive oxygen species (ROS), both of which contribute to heat-induced skeletal muscle injury. In this study, we tested whether either astaxanthin or quercetin, two dietary antioxidants, could ameliorate heat-induced skeletal muscle oxidative injury. In mouse C2C12 myoblasts exposed to 43°C heat stress, astaxanthin inhibited heat-induced ROS production in a concentration-dependent manner (1-20 μM), whereas the ROS levels remained high in cells treated with quercetin over a range of concentrations (2-100 µM). Because mitochondria are both the main source and a primary target of heat-induced ROS, we then tested the effects of astaxanthin and quercetin on mitochondrial integrity and function, under both normal temperature (37°C) and heat stress conditions. Quercetin treatment at 37°C induced mitochondrial fragmentation and decreased membrane potential (ΔΨ m ), accompanied by reduced protein expression of the master regulator of mitochondrial biogenesis peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). It also induced cleavage of mitochondrial inner-membrane fusion protein OPA1. In contrast, astaxanthin at 37°C increased protein expression of PGC-1α and mitochondrial transcription factor A (TFAM), and maintained tubular structure and normal ΔΨm . Under 43°C heat stress conditions, whereas quercetin failed to rescue C2C12 cells from injury, astaxanthin treatment prevented heat-induced mitochondrial fragmentation and depolarization, and apoptotic cell death. We also isolated rat flexor digitorum brevis myofibers and confirmed the data from C2C12 myoblasts that astaxanthin but not quercetin preserves mitochondrial integrity and function and ameliorates heat-induced skeletal muscle injury. These results confirm that mitochondria may be a potential therapeutic target for heat-related illness and suggest that astaxanthin may potentially be an effective preventive strategy.

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Published In

J Cell Physiol

DOI

EISSN

1097-4652

Publication Date

August 2019

Volume

234

Issue

8

Start / End Page

13292 / 13302

Location

United States

Related Subject Headings

  • Xanthophylls
  • Reactive Oxygen Species
  • Rats
  • Quercetin
  • Oxidative Stress
  • Myoblasts
  • Muscular Diseases
  • Mitochondria
  • Mice
  • Membrane Potential, Mitochondrial
 

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Yu, T., Dohl, J., Chen, Y., Gasier, H. G., & Deuster, P. A. (2019). Astaxanthin but not quercetin preserves mitochondrial integrity and function, ameliorates oxidative stress, and reduces heat-induced skeletal muscle injury. J Cell Physiol, 234(8), 13292–13302. https://doi.org/10.1002/jcp.28006
Yu, Tianzheng, Jacob Dohl, Yifan Chen, Heath G. Gasier, and Patricia A. Deuster. “Astaxanthin but not quercetin preserves mitochondrial integrity and function, ameliorates oxidative stress, and reduces heat-induced skeletal muscle injury.J Cell Physiol 234, no. 8 (August 2019): 13292–302. https://doi.org/10.1002/jcp.28006.
Yu, Tianzheng, et al. “Astaxanthin but not quercetin preserves mitochondrial integrity and function, ameliorates oxidative stress, and reduces heat-induced skeletal muscle injury.J Cell Physiol, vol. 234, no. 8, Aug. 2019, pp. 13292–302. Pubmed, doi:10.1002/jcp.28006.
Journal cover image

Published In

J Cell Physiol

DOI

EISSN

1097-4652

Publication Date

August 2019

Volume

234

Issue

8

Start / End Page

13292 / 13302

Location

United States

Related Subject Headings

  • Xanthophylls
  • Reactive Oxygen Species
  • Rats
  • Quercetin
  • Oxidative Stress
  • Myoblasts
  • Muscular Diseases
  • Mitochondria
  • Mice
  • Membrane Potential, Mitochondrial