Pulmonary exposure to diesel exhaust particles (DEP) has been associated with high levels of oxidized DNA in lung cells, whereas long-term oral DEP exposure appears to induce the DNA repair system with concomitant unaltered levels of oxidized DNA in the colon and liver of rats. Here we studied the generation of oxidatively damaged DNA in young wild type (WT) and oxoguanine DNA glycosylase 1 (OGGl) deficient mice after dietary exposure to 0 mg/kg, 0.8 mg/kg, or 8 mg/kg Standard Reference Material 1650 in the feed for 21 days. The ingestion of DEP did not increase the levels of 8-oxo-7,8-dihydro-2 '-deoxyguanosine and comet assay endpoints in terms of strand break, endonuclease 111, and formamidopyrimidine glycosylase (FPG) in the colon, liver, and lung tissue of WT or Oggl(-/-) mice. The level of OGGl mRNA could only be measured in WT mice and it was not increased by DEP feeding. On the contrary, the level of FPG sites was twofold higher in the liver and lung of Oggl(-/-) mice compared to the levels in the WT mice tissues. In conclusion, although Oggl(-/-) mice have high levels of oxidized guanine lesions, they do not appear to be markedly vulnerable to the genotoxicity by oral administration of DEP. (C) 2007 Elsevier Ireland Ltd. All rights reserved.