Papatheofanis F J
Department of Orthopaedics, University of Illinois, College of Medicine, Chicago.
J Biomed Mater Res. 1989 Jun;23(6):661-8. doi: 10.1002/jbm.820230609.
The cytotoxicity of methyl- and isobutyl-2-cyanoacrylate adhesives was determined using a rat polymorphonuclear leukocyte suspension. Cell degranulation increased and migration decreased on addition of the alkyl-2-cyanoacrylates to the suspension in a concentration-dependent manner. When acetylsalicylic acid or indomethacin, inhibitors of prostaglandin H synthase, were present, the cytotoxicity observed on addition of the adhesives to the leukocytes decreased up to eightfold in a dose-dependent manner as detected by trypan blue exclusion. Likewise, glutathione peroxidase and superoxide dismutase lowered such cytotoxicity resulting from the cyanoacrylates up to eight- and sevenfold, respectively. The data suggested that the adhesives may have generated lipid hydroperoxides that activated prostaglandin and thromboxane biosynthesis, and participated in membranal oxidation and lysis. Such a mechanism may contribute to understanding the thrombotic events associated with the necrosis observed on application of these adhesives to tissues in vivo.
使用大鼠多形核白细胞悬液测定了甲基 - 2 - 氰基丙烯酸酯和异丁基 - 2 - 氰基丙烯酸酯粘合剂的细胞毒性。向悬液中添加烷基 - 2 - 氰基丙烯酸酯后,细胞脱粒增加而迁移减少,且呈浓度依赖性。当存在前列腺素H合酶抑制剂乙酰水杨酸或吲哚美辛时,通过台盼蓝排斥法检测发现,向白细胞中添加粘合剂后观察到的细胞毒性以剂量依赖性方式降低高达八倍。同样,谷胱甘肽过氧化物酶和超氧化物歧化酶分别将氰基丙烯酸酯产生的这种细胞毒性降低了高达八倍和七倍。数据表明,这些粘合剂可能产生了脂质氢过氧化物,从而激活了前列腺素和血栓素的生物合成,并参与了膜氧化和溶解。这样的机制可能有助于理解在体内将这些粘合剂应用于组织时观察到的与坏死相关的血栓形成事件。