Commercial infant formulas, human milk, and lipid emulsions were analyzed for evidence of naturally occurring lipid peroxidation and for susceptibility to an in vitro oxidative challenge using neonatal rat lung, liver, or intestine homogenates. Peroxidation was assessed by quantitation of TBA reactants, diene conjugates, lipid peroxides, and ethane and pentane hydrocarbons. The peroxidation of commercial formulas and human milk was influenced by the nutrient composition, as PUFA and iron enhanced while vitamin E inhibited one or more of the peroxidation pathways. Formulas and lipid emulsions differed in their response to a biological oxidant challenge. Neither neonatal rat lung nor liver tissue were effective in peroxidizing the formula or human milk in vitro, but both formula and human milk were peroxidized by exposure to neonatal rat intestinal tissue. The lipid emulsion was readily peroxidized by neonatal rat lung, liver, and intestinal tissue. The influence of nutrition on survival in hyperoxia was also studied by exposing newborn rat pups to either air or greater than 95% oxygen in the course of feeding Ringer's lactate, Similac 24 + iron, human milk, or Intralipid 10%. The survival of newborn rat pups exposed to air or greater than 95% oxygen was affected by the type of diet received.