Liscum L
Department of Physiology, Tufts University School of Medicine, Boston, MA 02111.
Biochim Biophys Acta. 1990 Jun 28;1045(1):40-8. doi: 10.1016/0005-2760(90)90201-8.
Mammalian cells, cultured in the presence of serum lipoproteins, acquire cholesterol necessary for growth from the uptake and lysosomal hydrolysis of low-density lipoproteins (LDL). The mechanism(s) of intracellular transport of LDL-derived cholesterol from lysosomes to other cellular sites is unknown. In this study, various pharmacological agents were assessed for their ability to inhibit the movement of LDL-cholesterol from lysosomes to the plasma membrane. The only pharmacological agent tested in these experiments that specifically inhibited LDL-cholesterol movement was U18666A. Ketoconazole impaired the intracellular transport of LDL-cholesterol; however, ketoconazole also had a general effect on cholesterol movement, since it impeded the desorption of endogenously synthesized cholesterol into the medium. Other drugs that affected cholesterol movement appeared to be nonspecific. Cholesterol transport from lysosomes to plasma membranes was not significantly altered by agents that affect lysosomal function or cytoskeletal organization, as well as energy poisons and cycloheximide.
在血清脂蛋白存在的情况下培养的哺乳动物细胞，通过摄取和低密度脂蛋白（LDL）的溶酶体水解获得生长所需的胆固醇。LDL衍生的胆固醇从溶酶体到细胞其他部位的细胞内运输机制尚不清楚。在本研究中，评估了各种药理剂抑制LDL胆固醇从溶酶体向质膜移动的能力。在这些实验中测试的唯一特异性抑制LDL胆固醇移动的药理剂是U18666A。酮康唑损害了LDL胆固醇的细胞内运输；然而，酮康唑也对胆固醇移动有普遍影响，因为它阻碍了内源性合成胆固醇向培养基中的解吸。其他影响胆固醇移动的药物似乎是非特异性的。影响溶酶体功能或细胞骨架组织的试剂，以及能量毒物和环己酰亚胺，均未显著改变胆固醇从溶酶体到质膜的运输。
