L-Arg as a precursor of nitric oxide (NO) can be used in experiments to observe the action of NO. The present work is aimed at exploring the effect of oral administration of L-Arg on the ischemia-reperfusion (IR) damage of endothelial cells (EC) and the clearance of reaction oxygen species in the IR carotid artery. Cerium-marked cytochemical technique was used to localize the H2O2 product in endothelium. The area of Ce-H2O2 denseprecipitate on the lumen surface of damaged endothelium per length of artery wall (nm2/nm) was measured. It was found that the dense precipitate was decreased to 102.1±27.6 in rats drinking tap water containing 2.5% L-arginine for 3 days, much less than in control rats drinking tap water only (203.7±31.8, p<0.01). Furthermore, the IR damage of EC was relieved markedly. Drinking tap water containing D-Arg or L-Lys had no effects either on the amount of dense precipitate or on the EC damage. NG-nitro- L-arginine methyl ester, an inhibitor of NO synthase, decreased the effect of L-Arg markedly. These results indicate that L-Arg administration can reduce H2O2 production in the IR artery, and thus IR damage of EC is alleviated.