INTRODUCTIONHelicobacter pylori has been recognized as the major cause of gastritis and peptic ulcer diseases. [1][2][3] This bacterium has high urease enzyme activity, resulting in an abnormally high concentration of ammonia (NH 4 OH) in the stomach of infected patients. 3 Given that H. pylori-associated chronic active gastritis is characterized by the invasion of neutrophils into the gastric mucosa 1, 3, 4 and that neutrophils utilize the H 2 O 2 -myeloperoxidase-halide system to generate an oxidant capable of destroying a variety of mammalian cell targets as well as micro-organisms, 5,6 it is assumed that neutrophil-derived hypochlorous acid (HClO) interacts with NH 4 OH to generate cytotoxic monochloramine (NH 2 Cl). 7,8 Indeed, it has been demonstrated that NH 2 Cl plays a role in the pathogenesis of NH 4 OHinduced gastric lesions in rats. 9, 10 We have also reported that both endogenous and exogenous NH 2 Cl damage the gastric mucosa at much lower concentrations than NH 4 OH. 11,12 In addition, we have recently SUMMARY Background: It is well known that neutrophil-derived hypochlorous acid interacts with ammonia (NH 4 OH) to generate monochloramine (NH 2 Cl) and that NH 2 Cl irritates the gastric mucosa and impairs ulcer healing. Aim: To examine the effect of taurine, a hypochlorous acid scavenger, on the mucosal ulcerogenic and the impaired healing response induced by NH 2 Cl in rat stomachs, in comparison with those of methionine and glycine. Methods and results: Under anaesthesia, oral administration of NH 2 Cl (120 mmol/L) produced severe lesions in male Sprague-Dawley rat stomachs. Taurine (10-100 mg/kg) given p.o. 30 min prior to NH 2 Cl dosedependently prevented these lesions in response to NH 2 Cl. This action was mimicked by methionine (3-30 mg/kg) but not by glycine (10-100 mg/kg). Under urethane anaesthesia, mucosal exposure to NH 4 OH (120 mmol/L) caused a marked reduction of potential difference (PD) in the ex vivo chambered stomachs after