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金黄色葡萄球菌亚致死加热后耐盐性恢复的生理学研究

Pysiological studies on the recovery of salt tolerance by Staphylococcus aureus after sublethal heating.

作者信息

Hurst A, Hughes A, Beare-Rogers J L, Collins-Thompson D L

出版信息

J Bacteriol. 1973 Nov;116(2):901-7. doi: 10.1128/jb.116.2.901-907.1973.

Abstract

Cultures of S. aureus in 100 mM potassium phosphate buffer heated at 52 C for 15 min lost their tolerance to 7.5% NaCl. After incubation in a complex growth medium or in a diluted dialyzed medium in which unheated cells were unable to grow, salt tolerance was regained. Heat injury caused 30% loss of lipid. During recovery, the concentration of C(15) and C(17) fatty acids returned to normal, and there appeared to be an oversynthesis of C(16) and C(18) unsaturated acids. Penicillin abolished the latter reaction without affecting recovery; chloramphenicol did not affect fatty acid oversynthesis but reduced recovery. The K/Na ratio was 12.6 in control cells and 3.4 in injured cells, where it remained during the recovery of salt tolerance. Aspartate uptake was about 10% of the control level after injury and about 35% at recovery. Control cells grew without a lag on subculture, but injured cells which had regained their salt tolerance needed about 2 more h of incubation. Cells recovering with penicillin needed 6 more h, and cells recovering with chloramphenicol did not grow without a prolonged lag. Cells of S. aureus, therefore, may recover their salt tolerance while various membrane functions are still damaged.

摘要

在52℃下加热15分钟的100 mM磷酸钾缓冲液中的金黄色葡萄球菌培养物失去了对7.5% NaCl的耐受性。在复杂生长培养基或稀释透析培养基中培养后,未加热的细胞无法生长,但耐盐性得以恢复。热损伤导致30%的脂质损失。在恢复过程中,C(15)和C(17)脂肪酸的浓度恢复正常,并且似乎出现了C(16)和C(18)不饱和酸的过度合成。青霉素消除了后一种反应但不影响恢复;氯霉素不影响脂肪酸的过度合成但降低了恢复率。对照细胞的K/Na比为12.6,受损细胞为3.4,在耐盐性恢复过程中保持不变。损伤后天冬氨酸摄取量约为对照水平的10%,恢复时约为35%。对照细胞传代培养时无延迟生长,但恢复了耐盐性的受损细胞需要再培养约2小时。用青霉素恢复的细胞需要再培养6小时,用氯霉素恢复的细胞如果没有长时间的延迟则不生长。因此,金黄色葡萄球菌细胞在各种膜功能仍受损的情况下可能恢复其耐盐性。

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