Fishman P H, Curran P K
Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
FEBS Lett. 1992 Dec 21;314(3):371-4. doi: 10.1016/0014-5793(92)81508-j.
The fungal metabolite brefeldin A (BFA) is known to disrupt the Golgi apparatus resulting in redistribution of Golgi proteins to the endoplasmic reticulum and inhibition of protein secretion. BFA was found to inhibit protein synthesis in rat glioma C6 cells by up to 70% between 0.1 and 1 microgram/ml. Inhibition was both time-dependent and reversible. BFA inhibited protein synthesis to varying degrees in a number of other cell lines but not in BFA-resistant marsupial kidney cells. The same concentrations of BFA which inhibited protein synthesis, also blocked the inhibitory effects of Pseudomonas exotoxin and ricin on BFA-sensitive cells. BFA, however, was unable to block the inhibition of protein synthesis by the toxins in the resistant marsupial kidney cells.
真菌代谢产物布雷菲德菌素A（BFA）已知会破坏高尔基体，导致高尔基体蛋白重新分布到内质网，并抑制蛋白质分泌。研究发现，BFA在0.1至1微克/毫升的浓度范围内可使大鼠胶质瘤C6细胞中的蛋白质合成抑制高达70%。这种抑制作用具有时间依赖性且是可逆的。BFA在许多其他细胞系中也能不同程度地抑制蛋白质合成，但对BFA抗性有袋动物肾细胞无效。抑制蛋白质合成的相同浓度的BFA，也能阻断铜绿假单胞菌外毒素和蓖麻毒素对BFA敏感细胞的抑制作用。然而，BFA无法阻断毒素对有袋动物抗性肾细胞中蛋白质合成的抑制。
