Tachykinins stimulate lipid peroxidation mediated by free radicals in gastrointestinal tract of rat.

Tissue concentrations of malondialdehyde in the gastrointestinal tract of the rat were quantified as indicators of lipid peroxidation and tissue damage after challenge with tachykinins and after pretreatment with allopurinol. Neurokinin A, neurokinin B, and substance P given intravenously during 30 min increased the production of malondialdehyde in the stomach, duodenum, jejunum, and colon in a dose-dependent manner at doses from 100 to 400 pmol/kg/min (P < 0.05-0.01). However, the stomach seemed less responsive to the tachykinin challenge. For comparison, a similar dose-dependent increase of malondialdehyde was found in the liver and lung, with more pronounced effects of neurokinin B (P < 0.05-0.01). Pretreatment with allopurinol, 10 mg/kg, significantly reduced malondialdehyde responses to tachykinin challenge in intestinal tissues (P < 0.001). In conclusion, elaboration of malondialdehyde is suggested to reflect the ability of gastrointestinal tissues to react to tachykinins at high concentrations with liberation of free radicals as part of an inflammatory reaction.