Inhibition of vacuolation toxin activity of Helicobacter pylori by iodine, nitrite and potentiation by sodium chloride, sterigmatocystin and fluoride
Inhibition of vacuolation toxin activity of Helicobacter pylori by iodine, nitrite and potentiation by sodium chloride, sterigmatocystin and fluoride
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DOI：
10.1016/s0887-2333(02)00045-0
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发表时间：
2002-10-01
影响因子：
3.2
通讯作者：
Misumi, J
中科院分区：
文献类型：
--
作者：
Ma, FJ;Zhao, WY;Misumi, J
幽门螺杆菌产生的VacA毒素是决定幽门螺杆菌毒力的重要因素。VacA导致培养细胞(如HeLa细胞)出现空泡化。碘、亚硝酸盐、氯化钠、硫氰酸盐和真菌毒素杂色曲霉毒素在自然界中普遍存在，可能与胃癌的发生有关。本研究旨在检测上述化合物对VacA诱导的HeLa细胞空泡化的影响，并用中性红摄取实验对其进行定量。BafA1和NPPB可抑制VacA诱导的空泡化。碘、亚硝酸盐对大空泡的形成有抑制作用，而氯化钠、硫氰酸盐、氟化物和杂色曲霉毒素则促进大空泡的形成。我们的结果表明，VacA毒素可能与环境中自然存在的其他胃癌危险因素相互作用，并提示这些化合物可能调节Hp诱导的胃癌的发生发展。(C)2002爱思唯尔科学有限公司。保留所有权利。
The toxin VacA produced by Helicobacter pylori is an important determinant of virulence. VacA causes vacuolation of cultured cells such as HeLa cells. Iodine, nitrite, sodium chloride, thiocyanate and fungus toxin sterigmatocystin are universally present in nature and could possibly be related to carcinogenesis of the stomach. The present study was designed to examine the effects of the above-mentioned compound on VacA-induced vacuolation of HeLa cells, which was quantitated using the neutral red uptake assay. VacA-induced vacuolation was inhibited by BafA1 and NPPB. Formation of large vacuoles was inhibited in the presence of iodine, nitrite, but enhanced by sodium chloride, thiocyanate, fluoride and sterigmatocystin. Our results indicate that VacA toxin may interact with other gastric cancer risk factors present naturally in the environment, and suggest that those compounds may modulate the development of gastric cancer induced by H. pylori. (C) 2002 Elsevier Science Ltd. All rights reserved.