Acute tobacco smoke exposure promotes mitochondrial permeability transition in rat heart

Matt Eaton, Hemamalini Gursahani, Yehuda Arieli, Kent Pinkerton, Saul Schaefer

Research output: Contribution to journalArticlepeer-review


Chronic exposure to tobacco smoke is known to impair mitochondrial function. However, the effect of acute tobacco smoke exposure (ATSE) in vivo, as might occur in social settings, on mitochondrial function and calcium handling of cardiac cells has not been examined. It was hypothesized that ATSE might adversely modify mitochondrial function as reflected in mitochondrial energetics, membrane potential, and calcium transport. Mitochondria were isolated from the hearts of adult rats either exposed to 6 h of environmental tobacco smoke (∼60 mg/mm 3 tobacco smoke particles) or sham exposure. To model a calcium stress similar to ischemia/reperfusion, mitochondria were exposed to a Ca 2+ bolus with measurement of membrane potential, energetics, Ca 2+ uptake and release, and redox state. ATSE mitochondria were characterized by significantly higher ADP-stimulated ATP production and a more reduced redox state (NADH ratio) under basal conditions without observed changes in resting Ψ m. Exposure of ATSE mitochondria to Ca 2+ stress resulted in significantly more rapid depolarization of Ψ m. The initial rate of Ca 2+ uptake was not altered in ATSE mitochondria, but CsA-sensitive Ca 2+ release was significantly increased. ATSE does not significantly alter resting mitochondrial function. However, ATSE modifies the response of cardiac mitochondria to calcium stress, resulting in a more rapid depolarization and subsequent release of Ca 2+ via the mitochondrial permeability transition (MPT). Copyright

Original languageEnglish
Pages (from-to)1497-1510
Number of pages14
JournalJournal of Toxicology and Environmental Health - Part A: Current Issues
Issue number15
StatePublished - 2006
Externally publishedYes

Bibliographical note

Funding Information:
Received 21 March 2005; accepted 15 July 2005. This research was supported by a Philip Morris External Research program grant. We thank Mike Goldsmith and Dale Uyeminami at the Center for Health and Environment for invaluable assistance in the smoke exposure experiments. Address correspondence to Saul Schaefer, MD, One Shields Avenue, TB 172, Bioletti Way, University of California, Davis, Davis, CA 95616, USA. E-mail: [email protected]

ASJC Scopus subject areas

  • Health, Toxicology and Mutagenesis
  • Toxicology


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