Castiglione S, Paggi M G, Delpino A, Zeuli M, Floridi A
Laboratory for Cell Metabolism and Pharmacokinetics, Regina Elena Institute for Cancer Research, Rome, Italy.
Biochem Pharmacol. 1990 Sep 1;40(5):967-73. doi: 10.1016/0006-2952(90)90481-y.
The action of rhein, 4,5-dihydroxyanthraquinone-2-carboxylic acid, on protein synthesis of neoplastic cells has been investigated. Rhein decreases amino acid incorporation in all cells tested. The inhibition of incorporation of labeled precursors into acid-insoluble material cannot be ascribed to an impairment of amino acid uptake, which is unaffected by the drug. Tests on cell-free system showed that rhein does not inhibit the TMV-mRNA directed in vitro protein synthesis, thus indicating that the protein machinery per se is not affected. The inhibition of protein brought about by the drug must be ascribed to an effect on the energy-yielding processes with a remarkable decrease in ATP content. The mechanism is similar to that of other metabolic inhibitors, but rhein, for its capability to inhibit both respiration and glycolysis, is effective at much lower concentrations.
大黄酸（4,5-二羟基蒽醌-2-羧酸）对肿瘤细胞蛋白质合成的作用已得到研究。大黄酸降低了所有受试细胞中氨基酸的掺入。标记前体掺入酸不溶性物质的抑制作用不能归因于氨基酸摄取受损，因为该药物对此没有影响。对无细胞系统的测试表明，大黄酸不抑制烟草花叶病毒（TMV）-mRNA指导的体外蛋白质合成，因此表明蛋白质合成机制本身未受影响。该药物对蛋白质的抑制作用必定归因于对能量产生过程的影响，导致ATP含量显著降低。其作用机制与其他代谢抑制剂相似，但大黄酸由于能够同时抑制呼吸作用和糖酵解，在低得多的浓度下就有效。
