Tissue concentrations of malondialdehyde in thegastrointestinal tract of the rat were quantified asindicators of lipid peroxidation and tissue damage afterchallenge with tachykinins and after pretreatment with allopurinol. Neurokinin A, neurokinin B,and substance P given intravenously during 30 minincreased the production of malondialdehyde in thestomach, duodenum, jejunum, and colon in adose-dependent manner at doses from 100 to 400 pmol/kg/min (P< 0.05–0.01). However, the stomach seemed lessresponsive to the tachykinin challenge. For comparison,a similar dose-dependent increase of malondialdehyde was found in the liver and lung, with morepronounced effects of neurokinin B (P <0.05–0.01). Pretreatment with allopurinol, 10mg/kg, significantly reduced malondialdehyde responsesto tachykinin challenge in intestinal tissues (P < 0.001). Inconclusion, elaboration of malondialdehyde is suggestedto reflect the ability of gastrointestinal tissues toreact to tachykinins at high concentrations withliberation of free radicals as part of an inflammatoryreaction.