Farooqui M Y, Ahmed A E
Chem Biol Interact. 1982 Jan;38(2):145-59. doi: 10.1016/0009-2797(82)90036-9.
The interaction of acrylonitrile (VCN) with rat blood has been investigated at the molecular level in an attempt to understand the possible mechanism of its toxicity. The results obtained were compared to those with potassium cyanide (KCN), a compound known to liberate cyanide (CN-) in biologic conditions. The radioactivity derived from K14CN was eliminated faster than that from [1-14C]VCN. Up to a maximum of 94% of 14C from VCN in erythrocytes was detected covalently bound to cytoplasmic and membrane proteins, whereas 90% of the radioactivity from KCN in erythrocytes was found in the heme fraction of hemoglobin. Determination of specific activity showed that binding occurred more in vivo than in vitro which indicated that the VCN molecule was bioactivated inside erythrocytes. These results indicate that KCN interacts mainly through CN- liberation and binding to heme, whereas VCN, which binds to cytoplasmic and membrane proteins, may cause damage to red cells by mechanisms other than release of CN-.
已在分子水平上研究了丙烯腈（VCN）与大鼠血液的相互作用，以试图了解其毒性的可能机制。将所得结果与氰化钾（KCN）的结果进行了比较，KCN是一种已知在生物条件下会释放氰化物（CN-）的化合物。源自K14CN的放射性比源自[1-14C]VCN的放射性消除得更快。在红细胞中，高达94%的来自VCN的14C被检测到与细胞质和膜蛋白共价结合，而在红细胞中，90%的来自KCN的放射性存在于血红蛋白的血红素部分。比活度的测定表明，体内结合比体外更多，这表明VCN分子在红细胞内被生物活化。这些结果表明，KCN主要通过CN-的释放和与血红素的结合相互作用，而与细胞质和膜蛋白结合的VCN可能通过释放CN-以外的机制对红细胞造成损伤。
