Comparative evaluation of the effects of short-term inhalation exposure to diesel engine exhaust on rat lung and brain

Arch Toxicol. 2010 Jul;84(7):553-62. doi: 10.1007/s00204-010-0551-7. Epub 2010 May 14.

Abstract

Combustion-derived nanoparticles, such as diesel engine exhaust particles, have been implicated in the adverse health effects of particulate air pollution. Recent studies suggest that inhaled nanoparticles may also reach and/or affect the brain. The aim of our study was to comparatively evaluate the effects of short-term diesel engine exhaust (DEE) inhalation exposure on rat brain and lung. After 4 or 18 h recovery from a 2 h nose-only exposure to DEE (1.9 mg/m(3)), the mRNA expressions of heme oxygenase-1 (HO-1), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and cytochrome P450 1A1 (CYP1A1) were investigated in lung as well as in pituitary gland, hypothalamus, olfactory bulb, olfactory tubercles, cerebral cortex, and cerebellum. HO-1 protein expression in brain was investigated by immunohistochemistry and ELISA. In the lung, 4 h post-exposure, CYP1A1 and iNOS mRNA levels were increased, while 18 h post-exposure HO-1 was increased. In the pituitary at 4 h post-exposure, both CYP1A1 and HO-1 were increased; HO-1 was also elevated in the olfactory tuberculum at this time point. At 18 h post-exposure, increased expression of HO-1 and COX-2 was observed in cerebral cortex and cerebellum, respectively. Induction of HO-1 protein was not observed after DEE exposure. Bronchoalveolar lavage analysis of inflammatory cell influx, TNF-alpha, and IL-6 indicated that the mRNA expression changes occurred in the absence of lung inflammation. Our study shows that a single, short-term inhalation exposure to DEE triggers region-specific gene expression changes in rat brain to an extent comparable to those observed in the lung.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / metabolism
  • Cyclooxygenase 2 / metabolism
  • Cyclooxygenase 2 / pharmacology
  • Heme Oxygenase-1 / metabolism
  • Heme Oxygenase-1 / pharmacology
  • Inhalation Exposure*
  • Interleukin-6 / metabolism
  • Interleukin-6 / pharmacology
  • Lung / chemistry
  • Lung / drug effects
  • Lung / metabolism
  • Male
  • Nitric Oxide Synthase Type II / metabolism
  • Pneumonia / chemically induced
  • Pneumonia / metabolism
  • Rats
  • Rats, Inbred F344
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology
  • Vehicle Emissions / analysis*

Substances

  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Vehicle Emissions
  • NOS2 protein, human
  • Nitric Oxide Synthase Type II
  • Heme Oxygenase-1
  • Cyclooxygenase 2
  • PTGS2 protein, human