Stroev Serguei A, Gluschenko Tatjana S, Tjulkova Ekaterina I, Rybnikova Elena A, Samoilov Michail O, Pelto-Huikko Markku
Department of Developmental Biology, Tampere University Medical School and Department of Pathology, Tampere University Hospital, Tampere FIN-33014, Finland.
Neurosci Res. 2005 Sep;53(1):39-47. doi: 10.1016/j.neures.2005.05.010.
Severe hypoxia results in functional and structural injury of the brain. A preconditioning with repetitive episodes of mild hypoxia considerably ameliorates neuronal resistance to subsequent severe hypoxia. Activation of endogenous antioxidants including Cu, Zn-depending superoxide dismutase (Cu, Zn-SOD) (EC.1.15.1.1) is one of the main cell defense mechanisms against oxidative stress induced by hypoxia. Alterations of expression and enzyme activity of Cu, Zn-SOD 3 and 24h after severe hypobaric hypoxia in forebrain structures of preconditioned and non-preconditioned rats were investigated. We found that hypoxia without preconditioning suppressed the Cu, Zn-SOD enzyme activity at 3h time-point but preconditioning essentially modified the reaction to severe hypoxia by increasing the expression and activity of Cu, Zn-SOD during early stages of reoxygenation crucial for apoptosis initiation.
严重缺氧会导致大脑的功能和结构损伤。轻度缺氧的反复发作进行预处理可显著改善神经元对随后严重缺氧的耐受性。内源性抗氧化剂的激活，包括铜锌超氧化物歧化酶（Cu，Zn-SOD）（EC.1.15.1.1），是细胞抵抗缺氧诱导的氧化应激的主要防御机制之一。研究了预处理和未预处理大鼠在前脑结构中严重低压缺氧3小时和24小时后铜锌超氧化物歧化酶的表达和酶活性变化。我们发现，未预处理的缺氧在3小时时间点抑制了铜锌超氧化物歧化酶的酶活性，但预处理通过在对凋亡启动至关重要的复氧早期增加铜锌超氧化物歧化酶的表达和活性，从根本上改变了对严重缺氧的反应。
