Sidransky H, Verney E, Murty C N, Sarma D S, Reid M
Chem Biol Interact. 1977 Jul;18(1):69-82. doi: 10.1016/0009-2797(77)90142-9.
This study was concerned with the effect of aflatoxin B1 on protein synthesis in rat liver. Specifically, the effect of the administration of aflatoxin B1 (6.0 mg/kg body weight) on hepatic polyribosomes (free and membranebound), protein synthesis in vitro, and initiation factors activity of rats within 3-12 h was investigated. The results revealed that aflatoxin B1 rapidly led to disaggregation of free and membrane-bound polyribosomes, to inhibition of in vitro protein synthesis by both populations of polyribosomes, to little or no effect on the activities of initiation factors, and to defective ribosomes, particularly the 60S ribosomal subnits, of both types of polyribosomes. Comparative studies on the effects of aflatoxin B1 and actinomycin D revealed progressive disaggregation by both hepatic free and membrane-bound polyribosomes after aflatoxin B1 but not only of the free polyribosomes after actinomycin D.
本研究关注黄曲霉毒素B1对大鼠肝脏蛋白质合成的影响。具体而言,研究了给予黄曲霉毒素B1(6.0毫克/千克体重)对大鼠肝脏多核糖体(游离型和结合型)、体外蛋白质合成以及3至12小时内起始因子活性的影响。结果显示,黄曲霉毒素B1迅速导致游离型和结合型多核糖体解聚,抑制这两种多核糖体群体的体外蛋白质合成,对起始因子活性影响很小或无影响,并导致两种类型多核糖体出现核糖体缺陷,尤其是60S核糖体亚基。对黄曲霉毒素B1和放线菌素D作用的比较研究表明,黄曲霉毒素B1作用后肝脏游离型和结合型多核糖体均出现渐进性解聚,而放线菌素D作用后仅游离型多核糖体解聚。