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Helicobacter pylori NCTC 11637, which is nonviable at pH 3.0, became viable after addition of 10 mM urea owing to ammonia production by urease. In a buffer supplemented with urea, ecabet sodium decreased both the production of ammonia and the number of viable cells of H. pylori NCTC 11637 and changed the bacteria from the bacilliform to the horseshoe or doughnut shape in a concentration-dependent manner. In particular, ecabet sodium (2 and 4 mg/ml) decreased the number of viable cells below the control level. Benzohydroxamic acid, a urease inhibitor, also caused a decrease in ammonia production accompanied by a decrease in the number of viable cells and changed the morphological form at pH 3.0, but the number of viable cells was not lowered below the control level. In buffers at various pHs without urea, ecabet sodium showed a concentrationdependent bactericidal effect on H. pylori at pHs 4.0 and 5.0 but not at pHs 6.0 and 7.0 while benzohydroxamic acid caused only a slight decrease in the number of viable cells at pH 4.0. These results suggest that ecabet sodium has strong bactericidal activity in addition to its urease-inhibiting activity under acidic conditions.

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1-β-D-Arabinofuranosylcytosine (Ara-C), a cytidine analogue, inhibits DNA synthesis and is used for the treatment of myelogenous leukemia. On the other hand, it is also known that Ara-C has a teratogenic effect. In the present study, pregnant rats were treated with 250 mg/kg of Ara-C on day 13 of gestation, and fetal tissues and placentae were collected from 3 to 48 hours after treatment to examine the sequential histopathological changes induced by prenatal Ara-C treatment. The weights of fetuses and placentae and the thickness of the placental labyrinth zone were significantly reduced at 48 hours after treatment. In the fetal tissues such as central nervous system and mesenchymes and in the placental labyrinth zone, the number of pyknotic cells stained positively by the TUNEL method increased markedly after treatment with Ara-C. In most fetal tissues, the number began to increase from 3 to 6 hours and peaked at 9 to 12 hours after treatment. In the placental labyrinth zone, the number peaked at 6 hours after treatment. Electron microscopical features of the pyknotic cells consisted with the ultrastructural characteristics of apoptotic cells. In various fetal organs and placentae, abnormal induction of apoptosis is suggested to induce growth inhibition and have a certain relation to the malformations. Moreover, abnormal induction of apoptosis would have a deep connection with the cytotoxic effect of Ara-C which may affect proliferative cells in fetuses and placentae developing rapidly. (J Toxicol Pathol 2003; 16: 223-229)