In the industrial communities of today there is reason for concern for the reproductive health of the male, due to decreasing sperm quality and increased incidences of testicular cancer. Norway and Denmark have the highest incidence rates of testicular cancer in the world. There has traditionally been more focus on the maternal contribution for infertility and defects on the offspring compared to the paternal contribution. The genetic constitution of the offspring depends on the integrity of both the paternal (sperm) and the maternal (oocyte) genomes. When the integrity of the paternal genome is challenged it may lead to serious conditions; Oxidative damage in human sperm correlates with poor sperm quality and reduced fecundity (ability to conceive children). Couples undergoing assisted fertilisation have lower success rates when the father is a smoker, and there is epidemiological data suggesting that children of smoking fathers have a higher risk of developing cancer. One component of cigarette smoke, Benzo(a)pyrene (BaP), induce bulky DNA adducts and also is believed to cause oxidised base damage through generation of reactive oxygen species (ROS).BaP is a polycyclic aromatic hydrocarbon (PAH) that has been studied extensively. PAHs are an ubiquitous class of environmental contaminants. We are exposed to PAHs on a daily basis from food, burning of fossil fuels, forest fire, tobacco smoke and diesel exhaust. This exposure to humans qualifies for extensive studies to achieve a good understanding of the possible negative effects on humans.BaP-exposure leads to induction of DNA damage that may be removed via DNA repair. We have previously shown that human testicular cells exhibit poor repair of oxidative damage such as 8-oxoG, compared to rodents. We, and others, have also shown that male germ cells exhibit a low NER function for several bulky DNA adducts, including BPDE-adducts. These findings indicate that male germ cells, particularly human, may be particularly sensitive for exposure to certain environmental agents and that care should be taken in extrapolating results from rodents to man. The use of repair deficient mice, such as Ogg1-/- mice, thus mimics the repair capacity of human male germ cells and allows more relevant analyses of the possible genotoxic effects of environmental agents.In this study a small increase in oxidative damage was observed in the testis at Day 31 following BaP-exposure of Ogg1-/- mice. The increased levels of oxidative damage were most evident in haploid round spermatids. Oxidative damage was also induced in the somatic tissues investigated in Ogg1-/- mice; at Day 31 a small increase was observed in the liver whereas in the lung a more pronounced induction was detected, with increases at both Day 17 and Day 31 after exposure. No increases in oxidative damage were observed in Ogg1+/+ mice in any of the tissues investigated. NADP/NADPH-ratios declined following BaP-exposure in line with the DNA damage levels observed. The expression of Cyp1a1 and Akr1a4 was studied, with induction of Cyp1a1 at Day 1 following exposure in all tissues examined of both genotypes. The constitutive expression of Akr1a4 was significantly higher than Cyp1a1 in all the tissues. Akr1a4 was induced following BaP-exposure in the testis at Day 17 in Ogg1+/+ mice whereas the induction on the lung was more apparent, it occurred in both genotypes and took place at earlier time points following BaP-exposure. The decline in NADP/NADPH-ratios and expression levels of Cyp1a1 and Akr1a4 correspond well with the oxidative DNA damage levels observed. We conclude that exposure to BaP in vivo do induce oxidative damage. We provide solid evidence for its induction on the lung whereas the indications that oxidative damage is induced in male germ cells or in the liver are still unresolved.