Lorian V, Sabath L D, Simionescu M, Watson D W
Proc Soc Exp Biol Med. 1975 Jul;149(3):731-5. doi: 10.3181/00379727-149-38888.
The finding of reduced ribosomal densities at lower concentrations than those required to stop growth or cause visible defects in the cell wall is in contrast to the current view that the initial lesion produced by penicillins or cephalosporins is a defect in murein synthesis (11). This reduction in ribosomal density could be a primary or secondary effect and might be due to a decreased rate of growth, which has been shown to be associated with a lower ribosome frequency (12, 13) or to less stable ribosomes which disintegrated either spontaneously or as a result of the fixation procedures. The possibility that the decrease in ribosomal frequency was due to dilution (influx of liquid through a defective cell wall and/or cytoplasmic membrane, or efflux of ribosomes) remains, but no gross defect in cell wall was seen in more than 50 sections of cells showing reductions in ribosomal frequency. These findings suggest that an effect on ribosomes may antecede an effect on the cell wall.
在低于抑制生长或导致细胞壁出现可见缺陷所需浓度时核糖体密度降低,这一发现与目前认为青霉素或头孢菌素产生的初始损伤是胞壁质合成缺陷的观点形成对比(11)。核糖体密度的这种降低可能是原发性或继发性效应,可能是由于生长速率降低,已有研究表明生长速率降低与核糖体频率较低有关(12, 13),或者是由于核糖体稳定性较低,这些核糖体要么自发解体,要么因固定程序而解体。核糖体频率降低是由于稀释(液体通过有缺陷的细胞壁和/或细胞质膜流入,或核糖体流出)的可能性仍然存在,但在50多个显示核糖体频率降低的细胞切片中,未观察到细胞壁有明显缺陷。这些发现表明,对核糖体的影响可能先于对细胞壁的影响。