Aracena Paula, Aguirre Pabla, Muñoz Pablo, Núñez Marco T
Department of Biology, Faculty of Sciences and Cell Dynamic and Biotechnology Research Center, Universidad de Chile, Santiago, Chile.
Biol Res. 2006;39(1):157-65. doi: 10.4067/s0716-97602006000100017.
Neurons, as non-dividing cells, encounter a myriad of stressful conditions throughout their lifespan. In particular, there is increasing evidence that iron progressively accumulates in the brain with age and that iron induced oxidative stress is the cause of several forms of neurodegeneration. Here, we review recent evidence that gives support to the following notions: 1) neuronal iron accumulation leads to oxidative stress and cell death; 2) neuronal survival to iron accumulation associates with decreased expression of the iron import transporter DMT1 and increased expression of the efflux transporter IREG1; and 3) the adaptive process of neurons towards iron-induced oxidative stress includes a marked increase in both the expression of the catalytic subunit of gamma glutamate-cysteine ligase and glutathione. These findings may help to understand aging-related neurodegeneration hallmarks: oxidative damage, functional impairment and cell death.
神经元作为不分裂细胞,在其整个生命周期中会遇到无数应激条件。特别是,越来越多的证据表明,铁会随着年龄的增长在大脑中逐渐积累,并且铁诱导的氧化应激是多种神经退行性疾病的病因。在此,我们综述了最近的证据,这些证据支持以下观点:1)神经元铁积累导致氧化应激和细胞死亡;2)神经元对铁积累的存活与铁输入转运体DMT1表达降低和外流转运体IREG1表达增加相关;3)神经元对铁诱导的氧化应激的适应性过程包括γ-谷氨酰半胱氨酸连接酶催化亚基和谷胱甘肽的表达均显著增加。这些发现可能有助于理解与衰老相关的神经退行性疾病的特征:氧化损伤、功能障碍和细胞死亡。