Fischer 344 rats were injected with the spin traps C-phenyl N-tert-but
yl nitrone (PEN, 150 mg/kg bw, ip) or 4-pyridine-N-oxide N-tert-butyl
nitrone (POBN, 775 mg/kg bw, ip), and exposed to clean air or 2 ppm oz
one for two hours. The presence of spin adducts was determined by elec
tron paramagnetic resonance (EPR) spectroscopy of chloroform extracts
of lung and liver homogenates. No significant levels of adducts were d
etected in the lungs of air control animals. Benzoyl N-tert-butyl amin
oxyl, attributed to direct reaction of ozone with PEN, and tert-butyl
hydroaminoxyl, the scission product of the hydroxyl adduct of PEN, wer
e detected in the lungs of ozone exposed rats. EPR signals for cal-bon
-centred alkoxyl and alkyl adducts were also detected with PEN in the
lungs and liver of animals exposed to ozone. With POBN, only carbon-ce
ntred alkyl radicals were detected. Senescent, 24 months old rats were
found to retain about twice more (14)-C-PBN in blood, heart and lungs
by comparison to juvenile, 2 months old animals. Accordingly, the EPR
signals were generally stronger in the lungs of the senescent rats by
comparison to juvenile rats. Together, the observations were consiste
nt with the previously proposed notion that a significant flux of hydr
ogen peroxide produced from the reaction of ozone with lipids of the e
xtracellular lining, or from activated macrophages in the lungs could
be a source of biologically relevant amounts of hydroxyl radical.