ARIMA K, BEPPU M
J Bacteriol. 1964 Jul;88(1):143-50. doi: 10.1128/jb.88.1.143-150.1964.
Arima, Kei (University of Tokyo, Tokyo, Japan), and Michiko Beppu. Induction and mechanisms of arsenite resistance in Pseudomonas pseudomallei. J. Bacteriol. 88:143-150. 1964.-Pseudomonas pseudomallei strain 54, able to grow in the presence of 2 x 10(-2)m arsenite, was isolated from soil. After a short lag period, it grew at a normal growth rate. In the organisms grown with 10(-2)m arsenite, oxidation of alpha-ketoglutarate and other substrates proceeded in the presence of the same concentration of the drug. The concentration of arsenite which was half-inhibitory to alpha-ketoglutarate oxidation was 1.6 x 10(-3)m in the sensitive bacteria and 3.3 x 10(-2)m in the resistant ones. Cells capable of oxidizing alpha-ketoglutarate in the presence of arsenite were induced rapidly by contact with arsenite in growing cultures; when the drug was removed from the cultures, resistance was maintained for about two generations and then gradually disappeared. From the data presented, it was concluded that resistance in this organism is a physiological change and not a hereditary one. Further studies were carried out to investigate the arsenite-resistance mechanisms. alpha-Ketoglutarate dehydrogenase activity in the cell-free extracts of the resistant bacteria was sensitive to arsenite. An increase in the contents of this enzyme and sulfhydryl compounds, involving lipoic acid, was not observed in the resistant bacteria. The possibility of detoxication of arsenite was ruled out. Treatment of the resistant cells with cetyl-trimethylammonium bromide made them susceptible to 2 x 10(-2)m arsenite, although untreated cells were resistant to the same concentration of the drug. These data suggest the decreased permeability to arsenite of the resistant bacteria as a main mechanism of resistance.
有马圭(日本东京大学,东京)和别府美智子。类鼻疽杆菌对亚砷酸盐抗性的诱导及机制。《细菌学杂志》88:143 - 150。1964年。——从土壤中分离出能在2×10⁻²m亚砷酸盐存在下生长的类鼻疽杆菌菌株54。经过短暂的延迟期后,它以正常生长速率生长。在用10⁻²m亚砷酸盐培养的生物体中,α - 酮戊二酸和其他底物的氧化在相同浓度的药物存在下进行。对α - 酮戊二酸氧化具有半数抑制作用的亚砷酸盐浓度,在敏感细菌中为1.6×10⁻³m,在抗性细菌中为3.3×10⁻²m。在生长培养物中,能在亚砷酸盐存在下氧化α - 酮戊二酸的细胞通过与亚砷酸盐接触迅速被诱导;当从培养物中去除药物后,抗性维持约两代,然后逐渐消失。根据所呈现的数据得出结论,该生物体中的抗性是一种生理变化而非遗传变化。进行了进一步研究以探讨亚砷酸盐抗性机制。抗性细菌的无细胞提取物中的α - 酮戊二酸脱氢酶活性对亚砷酸盐敏感。在抗性细菌中未观察到该酶和涉及硫辛酸的巯基化合物含量增加。排除了亚砷酸盐解毒的可能性。用十六烷基三甲基溴化铵处理抗性细胞使其对2×10⁻²m亚砷酸盐敏感,尽管未处理的细胞对相同浓度的药物具有抗性。这些数据表明抗性细菌对亚砷酸盐的通透性降低是抗性的主要机制。