Type II I-compounds (indigenous DNA adducts) denote a class of bulky oxidative DNA lesions that are detectable by 32P-postlabeling and represent useful biomarkers of DNA damage induced by oxidative stress. Their levels are increased in tissue DNA under pro-oxidant conditions, for example, as previously shown, in newborn rat organs. Here we have investigated whether the maternal diet affects perinatal type II I-compound levels. Pregnant F344 rats were fed Purina-5001 natural-ingredient or AIN-93G purified diet from day 11 of gestation. Type II I-compounds were measured in liver DNA at three different developmental stages, i.e., fetus, and 24 h and 9 days postnatally. Higher adduct levels were detected in the Purina-5001 group at each stage. In a second experiment, pregnant F344 rats were subjected to dietary restriction (DR) (by 40%; Purina-5001) from day 12 of gestation. At 24 h postpartum hepatic type II I-compound levels were decreased compared to parallel ad libitum (AL) fed controls. As an unrelated observation, fetal lung, but not liver, kidney, and skin DNA contained a different pattern of nonpolar, apparently nonoxidative adducts, which were not diet-dependent. These spots were not detectable 24 h after birth and were observed at much reduced levels and only in a few samples at 9 days. The main results show for the first time that the maternal nutrition modulated levels of oxidative lesions in fetal and neonatal DNA, but the underlying mechanisms (e.g., differences in metal or caloric content of the diets) still need to be determined. The dietary effects were apparently transmitted through both placenta and the mother's milk.