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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Role of oxidative stress in the manganese and 1-methyl-4-(2'-ethylphenyl)-1,2,3,6-tetrahydropyridine-induced apoptosis in PC12 cells.
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Role of oxidative stress in the manganese and 1-methyl-4-(2'-ethylphenyl)-1,2,3,6-tetrahydropyridine-induced apoptosis in PC12 cells.

机译：氧化应激在锰和1-甲基-4-（2'-乙基苯基）-1,2,3,6-四氢吡啶诱导的PC12细胞凋亡中的作用。

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摘要

Oxidative stress is thought to play a key role in the apoptotic death of several cellular systems, including neurons. Oxidative stress is proposed also as a mechanism of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- and manganese (Mn)-induced neuronal death. We have recently shown that Mn and the MPTP analogue 1-methyl-4-(2'-ethylphenyl)-1,2,3,6-tetrahydropyridine (2'Et-MPTP), which is metabolized by MAO-A to 1-methyl-4-(2'-ethylphenyl)-pyridinium ion, induce apoptosis in PC12 cells. In the present study, we evaluated the effects of deprenyl and the antioxidant drugs N-acetylcysteine (NAC) and ascorbic acid (AA) on Mn- and 2'Et-MPTP-induced apoptosis in PC12 cells. Apoptosis was tested by terminal deoxynucleotidyl transferase-mediated 2'-deoxy-uridine-5'-triphosphate nick end labelling (TUNEL) technique, flow cytometry and fluorescence microscopy. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Mn-induced apoptosis and decrease in cell viability was inhibited by the antioxidants NAC and AA. Deprenyl failed to inhibit the above Mn effects. Neither NAC, AA nor deprenyl were able to inhibit both 2'Et-MPTP-induced apoptosis and decrease in cell viability. These results confirm that apoptosis may be an important mechanism of cell death in MPTP- and Mn-induced parkinsonism. However, an oxidative stress mechanism may be recognized, at least in vitro, only in the Mn-induced apoptosis.
机译：氧化应激被认为在包括神经元在内的几个细胞系统的凋亡死亡中起关键作用。还提出氧化应激作为神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）和锰（Mn）诱导的神经元死亡的机制。我们最近发现Mn和MPTP类似物1-甲基-4-（2'-乙基苯基）-1,2,3,6-四氢吡啶（2'Et-MPTP）被MAO-A代谢为1-甲基-4-（2'-乙基苯基）-吡啶鎓离子诱导PC12细胞凋亡。在本研究中，我们评估了异戊二烯基和抗氧化剂N-乙酰半胱氨酸（NAC）和抗坏血酸（AA）对Mn和2'Et-MPTP诱导PC12细胞凋亡的影响。通过末端脱氧核苷酸转移酶介导的2'-脱氧尿苷-5'-三磷酸缺口末端标记（TUNEL）技术，流式细胞仪和荧光显微镜检查细胞凋亡。细胞存活力通过3-（4,5-二甲基噻唑-2-基）-2,5-二苯基溴化四氮唑（MTT）测定来确定。锰诱导的细胞凋亡和细胞活力的降低被抗氧化剂NAC和AA抑制。异戊二烯基不能抑制上述Mn作用。 NAC，AA或异戊二烯基均不能抑制2'Et-MPTP诱导的凋亡并降低细胞活力。这些结果证实，凋亡可能是MPTP和Mn诱导的帕金森病中细胞死亡的重要机制。然而，至少在体外，仅在Mn诱导的细胞凋亡中可以认识到氧化应激机制。

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