Objective   To determine whether chronic exposure to cigarette smoke extract(CES)in mice could induce myocardium toxicity and to clarify whether nicotine in cigarette smoke is responsible for this impaired myocardium response.

  Methods   Transdermal injection of 50%, 40% CES 10 mg/kg twice daily or nicotine 1.5 mg/(kg°day)for 12 weeks.

  Results   Prolonged CSE administration caused a dose-dependent inhibition of cytochrome coxidase activity〔(424.75±66.25)vs (690.15±68.20)nmol/(mg°min), P < 0.01〕, while no significant changes in plasma GOT, LDH and CPK.Nicotine showed no significant damage on mouse heart mitochondria in vivo.Heart weight of the CSE-treated mice was significantly increased as compared with normal control group〔(0.29±0.05)vs(0.23±0.02)g, P < 0.05〕.The CSE exposure induced mitochondria was swollen with inner membrane damage, disruption of cristae, vacuolization of the matrix by transmission microscopy.

  Conclusion   Chronic exposure of mice to CSE caused inhibition of myocardial cytochrome C oxidase activity as well as mitochondrial structure damage.Nicotine was not the responsible component for the toxicity of CSE to myocardial mitochondria.