The aim of this study was to assess the role of nitric oxide (NO) in lipid peroxidation following 5 min of bilateral carotid occlusion in the Mongolian gerbil. The study consisted of 4 experimental groups (n = 10). Animals were either sham operated, subjected to bilateral carotid occlusion or administered the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg i.p.) 30 min, 6, 24 and 48 h following sham operation or 5 min bilateral carotid occlusion. Animals were killed 96 h post surgery and changes in the concentrations of malonaldehyde and 4 hydroxyalkenals (the main decomposition products of peroxides derived from polyunsaturated fatty acids and related esters) were measured in the hippocampus and cortex using the LPO-586 colorimetric method. The results showed a significant increase in the concentrations of both decomposition products following 5 min of bilateral carotid occlusion. L-NAME administered to sham operated controls had no effect, but in those animals subjected to 5 min of bilateral carotid occlusion L-NAME significantly decreased the levels of both decomposition products. These results suggest that inhibition of NO synthase activity decreases lipid peroxidation in the gerbil model of cerebral ischaemia.