Heipieper H J, de Bont J A
Department of Food Science, Wageningen Agricultural University, The Netherlands.
Appl Environ Microbiol. 1994 Dec;60(12):4440-4. doi: 10.1128/aem.60.12.4440-4444.1994.
Pseudomonas putida S12 was more tolerant to ethanol when preadapted to supersaturating concentrations of toluene. Cellular reactions at the membrane level to the toxicities of both compounds were different. In growing cells of P. putida S12, sublethal concentrations of toluene resulted in an increase in the degree of saturation of the membrane fatty acids, whereas toxically equivalent concentrations of ethanol led to a decrease in this value. Contrary to this, cells also reacted to both substances with a strong increase of the trans unsaturated fatty acids and a corresponding decrease of the cis unsaturated fatty acids under conditions where growth and other cellular membrane reactions were totally inhibited. While the isomerization of cis to trans unsaturated fatty acids compensates for the fluidizing effect caused by ethanol, a decrease in the degree of saturation is antagonistic with respect to the chemo-physical properties of the membrane. Consequently, the results support the hypothesis that the decrease in the degree of saturation induced by ethanol is not an adaptation mechanism but is caused by an inhibitory effect of the compound on the biosynthesis of saturated fatty acids.
恶臭假单胞菌S12在预先适应超饱和浓度的甲苯后,对乙醇的耐受性更强。细胞在膜水平上对这两种化合物毒性的反应有所不同。在恶臭假单胞菌S12的生长细胞中,亚致死浓度的甲苯会导致膜脂肪酸饱和度增加,而毒性相当的乙醇浓度则会使该值降低。与此相反,在生长和其他细胞膜反应完全受到抑制的条件下,细胞对这两种物质的反应都是反式不饱和脂肪酸大幅增加,顺式不饱和脂肪酸相应减少。虽然顺式不饱和脂肪酸向反式不饱和脂肪酸的异构化补偿了乙醇引起的膜流动性增加的效应,但饱和度的降低与膜的化学物理性质是拮抗的。因此,这些结果支持了这样一种假设,即乙醇诱导的饱和度降低不是一种适应机制,而是该化合物对饱和脂肪酸生物合成的抑制作用所致。