Shimura J, Shimura F, Hosoya N
Biochim Biophys Acta. 1985 Apr 22;845(1):43-7. doi: 10.1016/0167-4889(85)90052-7.
Rat splenocytes were provoked to lipid peroxidation in a dose-dependent manner by cumene hydroperoxide. After exposure to cumene hydroperoxide, formation of high molecular weight protein, presumably through cross-linking of lower molecular weight protein, was stimulated in splenocytes as well as in erythrocyte ghosts. The mitogenic response to concanavalin A of splenocytes was remarkably depressed by addition of cumene hydroperoxide to cultures. This depression was due rather to failures of splenocytes in responding to concanavalin A than deactivation of concanavalin A molecules. It is notworthy that the viability of splenocytes was unaffected by cumene hydroperoxide under the culture conditions where the mitogenic response was depressed. The addition of alpha-tocopherol or thiourea could block the depression of mitogenic response by cumene hydroperoxide, indicating that the depressed response to concanavalin A was related to radical formation. Overall evidence suggests that the function of immunocompetent cells can be depressed through lipid peroxidation-associated mechanisms without suffering from lethal damage.
氢过氧化异丙苯可使大鼠脾细胞发生脂质过氧化,且呈剂量依赖性。暴露于氢过氧化异丙苯后,脾细胞以及红细胞影中会刺激形成高分子量蛋白质,推测是通过低分子量蛋白质的交联形成的。向培养物中添加氢过氧化异丙苯会显著抑制脾细胞对刀豆球蛋白A的促有丝分裂反应。这种抑制相当程度上是由于脾细胞对刀豆球蛋白A无反应,而非刀豆球蛋白A分子失活。值得注意的是,在促有丝分裂反应受到抑制的培养条件下,氢过氧化异丙苯并未影响脾细胞的活力。添加α-生育酚或硫脲可阻止氢过氧化异丙苯对促有丝分裂反应的抑制,表明对刀豆球蛋白A反应的抑制与自由基形成有关。总体证据表明,免疫活性细胞的功能可通过脂质过氧化相关机制受到抑制,而不会遭受致命损伤。