Ribeiro-DaSilva G, Carlini C R, Pires-Barbosa R, Guimarães J A
Toxicon. 1986;24(8):775-82. doi: 10.1016/0041-0101(86)90102-9.
Canatoxin, a lethal convulsant protein isolated from the seeds of Canatoxin ensiformis (jack bean), induced a biphasic alteration in blood glucose levels when injected i.v. into rats and mice. After administration of subconvulsant doses of canatoxin the rats showed initially hyperglycemia during the first 30 min, followed by a long-lasting hypoglycemia. Return to basal glucose levels was not seen up to 15 days. The hyperglycemic effect was dose-dependent and occurred in starved and well-fed animals. A parallelism between convulsant and hyperglycemic activity was observed throughout all canatoxin purification steps. Mice were about 20-fold less sensitive (on a weight basis) than rats to canatoxin-induced hyperglycemia. The hyperglycemic phase was not affected by pretreatment of the rats with alpha- or beta-adrenergic blockers or chlorpromazine, but was potentiated by reserpine and haloperidol. Diazepam and hexamethonium were able to block the hyperglycemic phase of canatoxin's effect. The results suggest that the hyperglycemic alterations induced by canatoxin in rats and mice are probably mediated via the central nervous system.
刀豆毒素是从刀豆（洋刀豆）种子中分离出的一种致死性惊厥蛋白，静脉注射到大鼠和小鼠体内时会引起血糖水平的双相变化。给予亚惊厥剂量的刀豆毒素后，大鼠在最初30分钟内出现高血糖，随后是持续时间较长的低血糖。直到15天仍未恢复到基础血糖水平。高血糖作用呈剂量依赖性，在饥饿和饱食的动物中均会出现。在刀豆毒素的所有纯化步骤中，均观察到惊厥活性与高血糖活性之间存在平行关系。小鼠对刀豆毒素诱导的高血糖的敏感性（以体重计）比大鼠低约20倍。高血糖阶段不受用α-或β-肾上腺素能阻滞剂或氯丙嗪预处理大鼠的影响，但利血平和氟哌啶醇可增强该阶段。地西泮和六甲铵能够阻断刀豆毒素作用的高血糖阶段。结果表明，刀豆毒素在大鼠和小鼠中诱导的高血糖变化可能是通过中枢神经系统介导的。
