Fukuda N, Yamase T
Research Laboratory of Resources Utilization, Tokyo Institute of Technology, Yokohama, Japan.
Biol Pharm Bull. 1997 Aug;20(8):927-30. doi: 10.1248/bpb.20.927.
All of the vanadate and vanadyl compounds tested in this study showed potent antibacterial activity against Streptococcus pneumoniae: the MIC (minimum inhibitory concentration) values of the vanadium compounds were 4-32 micrograms/ml, while the MIC values of tungstates and molybdates were 128-->8000 micrograms/ml. Scanning electron microscopy showed the elongation of S. pneumoniae strains under low concentrations (< MIC) of vanadium compounds such as (tert-BuNH3)4[V4O12] (1), (tert-BuNH3)6[V10O28] (2), Na3VO4 (7) and VOSO4 (8). The vanadium compounds non-selectively inhibited the incorporation of thymidine, uridine, leucine and glucose into the cells of S. pneumoniae and led to an efflux of potassium ions from the cells. It implies that the vanadium compounds interfere in or on the cell membrane with the transport of substrates and ions through the cell membrane, resulting in antibacterial activity against S. pneumoniae cells.
钒化合物的最低抑菌浓度(MIC)值为4 - 32微克/毫升,而钨酸盐和钼酸盐的MIC值为128至8000微克/毫升。扫描电子显微镜显示,在低浓度(< MIC)的钒化合物如(叔丁基铵)4[V4O12](1)、(叔丁基铵)6[V10O28](2)、Na3VO4(7)和VOSO4(8)作用下,肺炎链球菌菌株出现伸长。钒化合物非选择性地抑制胸苷、尿苷、亮氨酸和葡萄糖掺入肺炎链球菌细胞,并导致钾离子从细胞外流。这意味着钒化合物干扰细胞膜上底物和离子的跨膜运输,从而对肺炎链球菌细胞产生抗菌活性。