Lead (Pb) exposure results in an increase in tissue lipid peroxides and variation in glutathione (GSH) concentrations, which can be related to peroxidative damage of cell membranes in Pb-poisoned animals. Species and individual variation in sensitivity to Pb poisoning among animals may be due to differential resistance to oxidative stress. The effects of oxidative stress caused by Pb exposure (1.7, 414, and 828 µg/g of diet) were compared for the first 6 wk in growing young of two species of waterfowl, Canada geese ( Branta canadensis ) and mallards ( Anas platyrhynchos ), with the first species being possibly more sensitive to Pb poisoning based on previous field and laboratory observations. Blood and liver Pb concentrations increased more in mallards than in geese. This may be explained on the basis of body weight, being 3.2 times higher in geese, and by hepatic metabolism, where GSH S -transferase (GST) activity is 2.9-fold higher in geese and presumably has a role in the binding of Pb to GSH and subsequent biliary excretion. In contrast, mallards showed higher hepatic levels of GSH and activities of GSH peroxidase (GPX) and GSH reductase (GR). Although both species showed a rise in hepatic GSH concentration with Pb exposure, the relationship between increased lipid peroxidation and Pb exposure was only significant in geese. Within treatment groups, hepatic GSH concentrations were inversely related to liver Pb concentrations in both species, which may correspond to the role of GSH in Pb excretion. Hepatic GSH was also inversely related to hepatic lipid peroxidation, but only in mallards and in agreement with the species differences observed in GPX and GR activities. The lower resistance to lipid peroxidation of Canada geese may explain why geese can die in the field from Pb poisoning after ingesting fewer shot than found in the gizzards of mallards and with lower liver Pb concentrations than in mallards.