Moore R A, Beckthold B, Bryan L E
Department of Microbiology and Infectious Diseases, University of Calgary Health Sciences Centre, Canada.
Can J Microbiol. 1995 Aug;41(8):746-9. doi: 10.1139/m95-102.
Currently, the mechanism of metronidazole resistance is not understood in Helicobacter pylori. We have looked at uptake of metronidazole into a sensitive and a resistant strain of H. pylori. Both strains displayed rapid uptake of [14C]metronidazole, although the resistant strain accumulated the drug at a slower rate and to a lesser amount than the sensitive strain. Uptake was inhibited by KCN and carbonyl cyanide m-chlorophenyl-hydrazone (CCCP) but not by sodium arsenate. Thin-layer chromatography analysis of lysed cell supernatants showed that metronidazole was metabolized in both strains. A variety of related imidazole compounds inhibited metronidazole uptake, consistent with a common transport system for this group of antibiotics. Our data do not support an absence of uptake or metabolism as a cause of resistance in the strain examined.
目前，幽门螺杆菌对甲硝唑耐药的机制尚不清楚。我们研究了甲硝唑在一株敏感和一株耐药幽门螺杆菌中的摄取情况。两株菌均对[14C]甲硝唑有快速摄取，尽管耐药菌株摄取药物的速度比敏感菌株慢，摄取量也比敏感菌株少。摄取受到氰化钾和羰基氰化物间氯苯腙（CCCP）的抑制，但不受砷酸钠的抑制。对裂解细胞上清液的薄层色谱分析表明，两株菌中甲硝唑均发生了代谢。多种相关咪唑化合物抑制甲硝唑摄取，这与这类抗生素存在共同转运系统一致。我们的数据不支持所检测菌株中摄取或代谢缺失是耐药原因的观点。
