Human mitochondrial oxidative capacity is acutely impaired after burn trauma

Melanie G. Cree, Ricki Y. Fram, David N. Herndon, Ting Qian, Carlos Angel, Justin M. Green, Ronald Mlcak, Asle Aarsland, Robert R. Wolfe

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


Background: Mitochondrial proteins and genes are damaged after burn injury in animals and are assessed in human burn patients in this study. Methods: The rates of maximal muscle mitochondrial oxidative capacity (adenosine triphosphate production) and uncoupled oxidation (heat production) for both palmitate and pyruvate were measured in muscle biopsies from 40 children sustaining burns on more than 40% of their body surface area and from 13 healthy children controls. Results: Maximal mitochondrial oxidation of pyruvate and palmitate were reduced in burn patients compared with controls (4.0 ± .2:1.9 ± .1 μmol O2/citrate synthase activity/mg protein/min pyruvate; control:burn; P < .001 and 3.0 ± .1:.9 ± .03 μmol O2/citrate synthase activity/mg protein/min palmityl CoA; control:burn; P = .003). Uncoupled oxidation was the same between groups. Conclusions: The maximal coupled mitochondrial oxidative capacity is severely impaired after burn injury, although there are no alterations in the rate of uncoupled oxidative capacity. It may be that the ratio of these indicates that a larger portion of energy production in trauma patients is wasted through uncoupling, rather than used for healing.

Original languageEnglish (US)
Pages (from-to)234-239
Number of pages6
JournalAmerican Journal of Surgery
Issue number2
StatePublished - Aug 2008


  • Burn
  • Mitochondria
  • Muscle
  • Trauma

ASJC Scopus subject areas

  • Surgery


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