Manoli L P, Gamaro G D, Silveira P P, Dalmaz C
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre, RS, Brazil.
Neurochem Res. 2000 Jul;25(7):915-21. doi: 10.1023/a:1007592022575.
It has been suggested that oxidative stress is involved in aging and neuropathologic disorders. In addition, chronic stress and high corticosterone levels are suggested to induce neuronal death. The aim of this study is to verify the effect of chronic variate stress on lipoperoxidation and on the total radical-trapping potential (TRAP) in hippocampus, hypothalamus and cerebral cortex. Adult male Wistar rats were submitted to different stressors during 40 days. Lipid peroxide levels were assessed by the thiobarbituric acid reactive species (TBARS) reaction, and TRAP was measured by the decrease in luminescence using the 2-2'-azo-bis(2-amidinopropane)-luminol system. The results showed that in cerebral cortex homogenates chronic stress induces an increase in oxidative stress. In hypothalamus a decreased lipoperoxidation was observed, however TRAP showed no difference. In hippocampus no difference was observed. We concluded that prolonged stress induces oxidative stress which varies selectively with the brain region.
有人提出氧化应激与衰老和神经病理障碍有关。此外，慢性应激和高皮质酮水平被认为会诱导神经元死亡。本研究的目的是验证慢性可变应激对海马体、下丘脑和大脑皮层中脂质过氧化和总自由基捕获能力（TRAP）的影响。成年雄性Wistar大鼠在40天内接受不同的应激源。通过硫代巴比妥酸反应性物质（TBARS）反应评估脂质过氧化物水平，并使用2-2'-偶氮双（2-脒基丙烷）-鲁米诺系统通过发光降低来测量TRAP。结果表明，在大脑皮层匀浆中，慢性应激会导致氧化应激增加。在下丘脑中观察到脂质过氧化减少，然而TRAP没有差异。在海马体中未观察到差异。我们得出结论，长期应激会诱导氧化应激，且氧化应激会因脑区不同而有选择性地变化。
