Shibanuma M, Kuroki T, Nose K
Biochem Biophys Res Commun. 1987 May 14;144(3):1317-23. doi: 10.1016/0006-291x(87)91454-9.
Serum, phorbol 12,13-didecanoate (PDD) and 1-oleoyl-2-acetoy-sn-glycerol (OAG) stimulated O2- release in human histiocytic leukemia U937 cells. The kinetics of O2- release caused by PDD but not by serum or OAG in growing cells differed from those in resting cells. Both the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl) 2-methylpiperidine (H-7) and calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) reduced the superoxide generation induced by these stimuli. H-7 inhibited the O2- release either from growing or resting cells but the effect of W-7 varied according to the growth phase. From these results, it is suggested that activation of protein kinase C and calmodulin-dependent process has an important role in O2(-)-release induced by serum, OAG and PDD, and that the mechanism for PDD-induced O2(-)-release is different in growing and resting cells.
血清、佛波醇12,13 - 二癸酸酯（PDD）和1 - 油酰基 - 2 - 乙酰基 - sn - 甘油（OAG）可刺激人组织细胞白血病U937细胞释放超氧阴离子（O₂⁻）。在生长细胞中，由PDD而非血清或OAG引起的O₂⁻释放动力学与静息细胞中的不同。蛋白激酶C抑制剂1 -（5 - 异喹啉磺酰基）- 2 - 甲基哌啶（H - 7）和钙调蛋白拮抗剂N -（6 - 氨基己基）- 5 - 氯 - 1 - 萘磺酰胺（W - 7）均可减少这些刺激诱导的超氧化物生成。H - 7抑制生长细胞或静息细胞释放O₂⁻，但W - 7的作用因生长阶段而异。从这些结果表明，蛋白激酶C的激活和钙调蛋白依赖性过程在血清、OAG和PDD诱导的O₂⁻释放中起重要作用，并且PDD诱导的O₂⁻释放在生长细胞和静息细胞中的机制不同。
