UDP-galactosyltransferase (UDP-Gal-T) is a key enzyme in the synthesis of mucus glycoproteins, which play an important role in gastric mucosal defensive mechanisms. Helicobacter pylori (HP) induces gastritis and peptic ulceers but mechanisms of HP-induced mucosal injury sre not fully understood. To elucidate the mechanism whereby (HP) infection induces gastric mucosal injury, we investigated the effects HP on the gastric mucosal defensive mechanism by measuring UDP-Gal T activies in HGC-27, a mucin-producing gastric caneer cell line, treated with various HP-relatd materials (sonicated HP, HP culture supernatants, live HP). HP-related materials induced no significant chages in UDP-Gal T activity, but the enzyme increased when we generated a low concentration of ammonia by adding sonicated HP. and urea simultaneousy. In contrast, UDP-Gal-T activity did not increase when we added live HP instead of sonicated HP. Next, we investigated the effects of HP on ethanol-induced injury in the HGC-27 cells. Pretreatment with ammonia of a low concetration significantly protected cells from ethanol-induced injury. In contrast, pretreatment with live HP and urea generated ammonia of the similar concentration but did not protect cells from the injoy. Our findings that HP has an inhibitory effect against adaptive cytoprotection induced by ammonia by inhibiting the induction of UDP-Gal T.