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低浓度青霉素G导致脑膜炎奈瑟菌细胞死亡和裂解的相关事件。

Events leading to cell death and lysis of Neisseria meningitidis in low concentrations of penicillin G.

作者信息

Neirinck L G, DeVoe I W, Ingram J M

出版信息

Antimicrob Agents Chemother. 1980 Apr;17(4):715-24. doi: 10.1128/AAC.17.4.715.

Abstract

Neisseria meningitidis SD1C exhibited a low tolerance to penicillin G (0.03 microgram/ml). Loss of viability in the absence of polyvinylpyrrolidone-40 and horse serum was independent of the concentration of antibiotic above the minimum inhibitory concentration, whereas the rate of bacteriolysis was concentration dependent. Penicillin-induced lysis was a secondary event in this organism. At low levels of penicillin G, growth characteristics, i.e., absorbancy changes, respiratory rate, and uptake of Mg2+, appeared normal during the first 90 min in penicillin; however, viability dropped dramatically. Additionally, total cell numbers remained constant while cell mass continued to increase at a rate normal for the population. The increase in cellular mass in the absence of cell division could be observed microscopically. Only one ultrastructural change induced by penicillin correlated with the loss in viability: the loss in continuity of the outer membrane with the peptidoglycan but only at the site of septum formation. This lesion did not occur when cells were grown in media supplemented with the protective agents polyvinylpyrrolidone-40 and horse serum. Under these conditions of growth and with relatively high levels of penicillin, constant viability was maintained, but cell division no longer occurred. Cell populations treated with penicillin in the presence of the protective agents became increasingly more dependent on the presence of these agents for total viability even in the absence of penicillin in the culture.

摘要

脑膜炎奈瑟菌SD1C对青霉素G耐受性低(0.03微克/毫升)。在没有聚乙烯吡咯烷酮-40和马血清的情况下,活力丧失与高于最低抑菌浓度的抗生素浓度无关,而细菌溶解速率则与浓度有关。青霉素诱导的溶解是该生物体中的次要事件。在低水平的青霉素G作用下,在青霉素作用的最初90分钟内,生长特性,即吸光度变化、呼吸速率和镁离子摄取,看起来是正常的;然而,活力急剧下降。此外,总细胞数保持不变,而细胞质量继续以群体正常速率增加。在没有细胞分裂的情况下细胞质量的增加可以通过显微镜观察到。青霉素诱导的唯一超微结构变化与活力丧失相关:外膜与肽聚糖的连续性丧失,但仅在隔膜形成部位。当细胞在添加了保护剂聚乙烯吡咯烷酮-40和马血清的培养基中生长时,这种损伤不会发生。在这些生长条件下以及相对高水平的青霉素作用下,活力得以维持,但细胞不再分裂。在存在保护剂的情况下用青霉素处理的细胞群体,即使在培养物中不存在青霉素时,其总活力也越来越依赖于这些保护剂的存在。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6f8/283858/f13674307d4b/aac00384-0207-a.jpg

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