School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, Korea.
BMB Rep. 2011 May;44(5):312-6. doi: 10.5483/BMBRep.2011.44.5.312.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its toxic metabolite 1-methyl-4-phenylpyridium ion (MPP(+)) have been shown to induce Parkinson's disease-like symptoms as well as neurotoxicity in humans and animal species. Recently, we reported that maintenance of redox balance and cellular defense against oxidative damage are primary functions of the novel antioxidant enzyme cytosolic NADP(+) -dependent isocitrate dehydrogenase (IDPc). In this study, we examined the role of IDPc in cellular defense against MPP(+) -induced oxidative injury using PC12 cells transfected with IDPc small interfering RNA (siRNA). Our results demonstrate that MPP(+) -mediated disruption of cellular redox status, oxidative damage to cells, and apoptotic cell death were significantly enhanced by knockdown of IDPc.
1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）及其有毒代谢物 1-甲基-4-苯基吡啶鎓离子（MPP(+)）已被证明可诱导人类和动物物种出现类似帕金森病的症状以及神经毒性。最近，我们报道称，新型抗氧化酶细胞质 NADP(+)依赖性异柠檬酸脱氢酶（IDPc）的主要功能是维持氧化还原平衡和细胞对氧化损伤的防御。在这项研究中，我们使用转染了 IDPc 小干扰 RNA（siRNA）的 PC12 细胞，研究了 IDPc 在细胞防御 MPP(+)诱导的氧化损伤中的作用。我们的结果表明，IDPc 的敲低显著增强了 MPP(+)介导的细胞氧化还原状态的破坏、细胞的氧化损伤和凋亡性细胞死亡。
