Nunn W D
Biochim Biophys Acta. 1975 Mar 24;380(3):403-13. doi: 10.1016/0005-2760(75)90108-3.
The kinetics of lipid metabolism during phenethyl alcohol treatment of Escherichia coli were examined. Phenethyl alcohol at a non-bacteriostatic concentration reduces the accumulation of [32-P] phosphate into phospholipids and alters the phospholipid composition of the cell membrane. The changes in phospholipid composition are a result of the inhibitory effect of phenethyl alcohol on the rates of synthesis of the individual phospholipids. The inhibition in the rate of phosphatidylethanolamine synthesis by phenethyl alcohol was twice the inhibition in the rate of phosphatidyglycerol synthesis. The de novo rate of cardiolipin synthesis was only slightly inhibited. However, net cardiolipin accumulation increased during phenethyl alcohol treatment due to a more rapid turnover of phosphatidylglycerol to cardiolipin. Phenethyl alcohol also altered the fatty acid composition of the cell as a result of its inhibitory effect on the rate of individual fatty acid synthesis. However, the inhibition of phospholipid synthesis was not reversed by fatty acid supplementation of phenethyl alcohol treated cells. This result indicates that phenethyl alcohol does not inhibit phospholipid synthesis solely at the level of fatty acid synthesis.
研究了苯乙醇处理大肠杆菌过程中脂质代谢的动力学。非抑菌浓度的苯乙醇会减少[32-P]磷酸盐向磷脂中的积累，并改变细胞膜的磷脂组成。磷脂组成的变化是苯乙醇对各磷脂合成速率产生抑制作用的结果。苯乙醇对磷脂酰乙醇胺合成速率的抑制是对磷脂酰甘油合成速率抑制的两倍。心磷脂的从头合成速率仅受到轻微抑制。然而，在苯乙醇处理期间，由于磷脂酰甘油向心磷脂的周转更快，心磷脂的净积累增加。由于苯乙醇对各脂肪酸合成速率的抑制作用，它还改变了细胞的脂肪酸组成。然而，对经苯乙醇处理的细胞补充脂肪酸并不能逆转对磷脂合成的抑制。这一结果表明，苯乙醇并非仅在脂肪酸合成水平上抑制磷脂合成。
