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Myofibrillar protein oxidation and contractile dysfunction in hyperthyroid rat diaphragm.

Takashi Yamada1, Takaaki Mishima, Makoto Sakamoto

  • 1Graduate School of Integrated Arts and Sciences, Hiroshima University, Japan 739-8521.

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 17, 2007
PubMed
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Thyroid hormone (T3) impairs diaphragm muscle function by oxidizing myofibrillar proteins. Antioxidant carvedilol treatment improved muscle force and prevented T3-induced protein oxidation in hyperthyroidism.

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Area of Science:

  • Physiology
  • Biochemistry
  • Endocrinology

Background:

  • Hyperthyroidism is associated with muscle dysfunction.
  • Thyroid hormones can influence protein metabolism and oxidative stress.

Purpose of the Study:

  • To investigate if thyroid hormone (3,5,3'-triiodo-L-thyronine, T3) causes myofibrillar protein oxidation and respiratory muscle dysfunction.
  • To evaluate the potential protective effects of carvedilol, an antioxidant beta-blocker.

Main Methods:

  • Rats were injected with T3 daily for 21 days.
  • Isometric forces of diaphragm fiber bundles were measured at various stimulus frequencies.
  • Myofibrillar protein carbonyl content was assessed.
  • The effects of carvedilol treatment were examined.

Main Results:

  • T3 administration significantly reduced diaphragm fiber bundle force production.
  • T3 treatment led to a significant increase in myofibrillar protein carbonyl groups.
  • Carvedilol treatment improved isometric tetanic force and prevented T3-induced protein oxidation.

Conclusions:

  • Oxidative modification of myofibrillar proteins contributes to diaphragm impairment in hyperthyroidism.
  • Carvedilol demonstrates potential therapeutic benefits by mitigating T3-induced muscle dysfunction and oxidative stress.