Both, developmental lead (Pb) exposure and ethanol intakeinduce reactive oxygen species (ROS), thus modifying the activity ofantioxidant enzymes such as catalase -CAT, superoxide dismutase -SOD, andglutathione peroxidase  -GPx. Importantly, CAT is also implicated inethanol?s brain oxidation to acetaldehyde. Based on these evidences, the aim ofthis study was to evaluate whether perinatal low-level Pb exposure would modifythe activity of these enzymes in male Wistar rats that have voluntarilyconsumed ethanol. Briefly, 35 day-old rats exposed to water or 220 ppm Pbduring gestation and lactation were presented 2h daily with increasing ethanol solutions(2-10%), and water until postnatal day 63 (group 63d ETOH). Another two groupswere included:  35d non-ETOH, and 63d non-ETOH. At the end of theexperiment, all animals were sacrificed, blood, and liver removed to determinethe activity of the antioxidant enzymes above-mentioned. All three enzymes(CAT, SOD and GPx) were increased in blood selectively in the 35d non-ETOHgroup perinatally exposed to Pb, whereas only CAT was further increased in the63d ETOH Pb-exposed group. On the other side, liver SOD activity was decreasedin the 35d non-ETOH and 63d non-ETOH Pb-exposed groups, whereas liver CATactivity was reduced in the 63d ETOH and 63d non-ETOH Pb-exposed groups. Nochanges were observed in liver GPx activity. These results suggest differentialantioxidant enzymatic activity probably determined by the dynamic Pbtoxicokinetics in blood and soft tissue, with CAT playing a critical role inthe Pb/ethanol interaction