Ennamany R, Bingen A, Creppy E E, Kretz O, Gut J P, Dubuisson L, Balabaud C, Bioulac Sage P, Kirn A
Université de Bordeaux II, Unité de Formation et de Recherche des Sciences Pharmaceutiques, France.
Hum Exp Toxicol. 1998 Nov;17(11):620-4. doi: 10.1177/096032719801701106.
Bolesatine is a toxic glycoprotein isolated from Boletus satanas Lenz, which inhibits protein synthesis in vivo and in vitro. The LD50 (24 h) is 1 mg /kg bw (i.p.), in mice and rats. When given i.p. to mice (0.1 - 1.0 mg/kg bw) bolesatine induced thrombi and blood stasis in the liver, 5 - 21 h after injection, and modifications of the number of blood corpuscles in peripheral blood. These effects were efficiently reversed by aspirin, ticlopidin and heparin (as attested by histology and electron microscopy) which however failed to prevent death in animals given lethal doses. Together, these results showed that the death of bolesatine poisoned animals given high doses, was rather due to a combination of thrombosis and other toxic effects. In addition, they suggest that these antithrombotic drugs may overcome cases of human poisoning, with low exposures of this boletus, showing a hypertension probably due to mechanical obstruction which resists normal therapy.
鬼笔毒素是从毒红菇中分离出的一种毒性糖蛋白，它在体内和体外均能抑制蛋白质合成。小鼠和大鼠的腹腔注射半数致死量（24小时）为1毫克/千克体重。给小鼠腹腔注射（0.1 - 1.0毫克/千克体重）鬼笔毒素后，在注射后5 - 21小时可诱导肝脏出现血栓和血瘀，并使外周血中的血细胞数量发生改变。阿司匹林、噻氯匹定和肝素可有效逆转这些作用（组织学和电子显微镜证实），但这些药物无法防止给予致死剂量的动物死亡。综合这些结果表明，高剂量鬼笔毒素中毒动物的死亡，更多是由于血栓形成和其他毒性作用共同导致的。此外，这些结果表明，这些抗血栓药物可能会治愈低剂量接触这种红菇而中毒的人类病例，这些病例可能表现为因机械性阻塞导致的高血压，常规治疗对此无效。
