Ray B, Speck M L
Appl Microbiol. 1972 Oct;24(4):585-90. doi: 10.1128/am.24.4.585-590.1972.
After Escherichia coli was injured by freezing, the repair process was studied during incubation of the cells for 2 hr at 25 C in 0.5% K(2)HPO(4) at pH 7.0 in the presence of specific metabolic inhibitors. The repair in K(2)HPO(4) was not affected by inhibitors of the synthesis of protein, nucleic acids, and mucopeptide. These inhibitors prevented growth of the repaired cells in a minimal broth at 35 C for 24 hr (except actinomycin D and hydroxyurea). Several uncouplers of adenosine triphosphate (ATP) synthesis reduced the repair process in K(2)HPO(4), but only cyanide and azide prevented growth in minimal medium. Data indicated that the cells synthesized energy in the form of ATP and probably utilized it for the repair process. Addition of ATP also facilitated the repair of injury. The freeze-injured cells showed extreme susceptibility to surface-active agents and lysozyme. The repaired cells, like the uninjured cells, became relatively resistant to these compounds.
大肠杆菌经冷冻损伤后,在特定代谢抑制剂存在的情况下,于25℃在pH 7.0的0.5%磷酸氢二钾(K₂HPO₄)中孵育细胞2小时,研究其修复过程。在磷酸氢二钾中的修复不受蛋白质、核酸和粘肽合成抑制剂的影响。这些抑制剂可阻止修复后的细胞在35℃的基本肉汤中生长24小时(放线菌素D和羟基脲除外)。几种三磷酸腺苷(ATP)合成解偶联剂降低了在磷酸氢二钾中的修复过程,但只有氰化物和叠氮化物可阻止在基本培养基中的生长。数据表明,细胞以ATP的形式合成能量,并可能将其用于修复过程。添加ATP也促进了损伤的修复。冷冻损伤的细胞对表面活性剂和溶菌酶表现出极高的敏感性。修复后的细胞与未损伤的细胞一样,对这些化合物变得相对耐受。