Cardiac mitochondrial damage and loss of ROS defense after burn injury: The beneficial effects of antioxidant therapy

Qun Zang, David L. Maass, Jean White, Jureta W. Horton

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Mechanisms of burn-related cardiac dysfunction may involve defects in mitochondria. This study determined 1) whether burn injury alters myocardial mitochondrial integrity and function; and 2) whether an antioxidant vitamin therapy prevented changes in cardiac mitochondrial function after burn. Sprague-Dawley rats were given a 3° burn over 40% total body surface area and fluid resuscitated. Antioxidant vitamins or vehicle were given to sham and burn rats. Mitochondrial and cytosolic fractions were prepared from heart tissues at several times postburn. In mitochondria, lipid peroxidation was measured to assess oxidative stress, mitochondrial outer membrane damage and cytochrome-c translocation were determined to estimate mitochondrial integrity, and activities of SOD and glutathione peroxidase were examined to evaluate mitochondrial antioxidant defense. Cardiac function was measured by Langendorff model in sham and burn rats given either vitamins or vehicle. Twenty-four hours postburn, mitochondrial outer membrane damage was progressively increased to ∼50%, and cytosolic cytochrome-c gradually accumulated to approximately three times more than that measured in shams, indicating impaired mitochondrial integrity. Maximal decrease of mitochondrial SOD activity occurred 8 h postburn (∼63.5% of shams), whereas maximal decrease in glutathione peroxidase activity persisted 2-24 h postburn (∼60% of shams). In burn animals, lipid peroxidation in cardiac mitochondria increased 30-50%, suggesting burn-induced oxidative stress. Antioxidant vitamin therapy prevented burn-related loss of membrane integrity and antioxidant defense in myocardial mitochondria and prevented cardiac dysfunction. These data suggest that burn-mediated mitochondrial dysfunction and loss of reactive oxygen species defense may play a role in postburn cardiac dysfunction.

Original languageEnglish (US)
Pages (from-to)103-112
Number of pages10
JournalJournal of Applied Physiology
Volume102
Issue number1
DOIs
StatePublished - Jan 2007

Fingerprint

Burns
Vitamins
Antioxidants
Wounds and Injuries
Mitochondria
Mitochondrial Membranes
Glutathione Peroxidase
Cytochromes c
Lipid Peroxidation
Oxidative Stress
Therapeutics
Heart Mitochondria
Body Surface Area
Sprague Dawley Rats
Reactive Oxygen Species
Membranes

Keywords

  • Burn trauma
  • Cardiac function
  • Mitochondria

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Cardiac mitochondrial damage and loss of ROS defense after burn injury : The beneficial effects of antioxidant therapy. / Zang, Qun; Maass, David L.; White, Jean; Horton, Jureta W.

In: Journal of Applied Physiology, Vol. 102, No. 1, 01.2007, p. 103-112.

Research output: Contribution to journalArticle

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