Laboratory of Molecular Biology and Endocrinology, Institute of Nuclear Science Vinča, University of Belgrade, Belgrade, Serbia.
Mol Cell Biochem. 2011 Nov;357(1-2):143-50. doi: 10.1007/s11010-011-0884-4. Epub 2011 May 29.
Exposure to different stressors initiates generation of reactive oxygen species (ROS), which create harmful environment for cellular macromolecules. Superoxide dismutases (SODs) represent the first line of antioxidant defense. Hence, any alternation in their function might be potentially damaging. To better define the role of SODs, we investigated the CuZnSOD activity in cytosolic and the nuclear fraction as well as mitochondrial MnSOD activity in the liver of Wistar male rats after exposure to 2 h of acute immobilization (IM) or cold (4°C) stress, 21 days of chronic social isolation (IS) or their combination (chronic stress followed by acute stress). Serum corticosterone (CORT) was monitored as an indicator of the stress response. Acute IM stress, with elevated CORT level, led to increased hepatic CuZnSOD activity in the nuclear fraction. Chronic isolation stress, where CORT was close to control value, did not change the CuZnSOD activity either in nuclei or in cytosolic fraction, while combined stress IS+Cold led to increased cytosolic CuZnSOD activity. MnSOD activity in mitochondrial fraction was decreased in all treated groups. Data have shown that different stressors have diverse effect on hepatic CuZnSOD and MnSOD activity as well as on serum CORT level. Increased nuclear CuZnSOD activity after acute stress represents physiological response since the named activity protects cells against oxidative stress, while chronic IS stress compromises CuZnSOD function, suggesting an inefficient defense against ROS. Observed decrease of MnSOD activities indicate inadequate elimination of ROS after acute or chronic stress, which is characteristic of the oxidative stress.
暴露于不同的应激源会引发活性氧（ROS）的产生，从而对细胞大分子造成有害环境。超氧化物歧化酶（SODs）是抗氧化防御的第一道防线。因此，其功能的任何改变都可能是潜在的有害的。为了更好地定义 SOD 的作用，我们研究了 Wistar 雄性大鼠在急性束缚（IM）或冷（4°C）应激 2 小时、21 天慢性社交隔离（IS）或其组合（慢性应激后急性应激）后，细胞溶质和核部分的 CuZnSOD 活性以及线粒体 MnSOD 活性。血清皮质酮（CORT）被监测为应激反应的指标。急性 IM 应激，CORT 水平升高，导致肝细胞核 CuZnSOD 活性增加。慢性隔离应激，CORT 接近对照值，无论是在核还是细胞溶质部分，CuZnSOD 活性都没有变化，而联合应激 IS+Cold 导致细胞溶质 CuZnSOD 活性增加。线粒体部分的 MnSOD 活性在所有处理组中均降低。数据表明，不同的应激源对肝 CuZnSOD 和 MnSOD 活性以及血清 CORT 水平有不同的影响。急性应激后核内 CuZnSOD 活性增加代表生理反应，因为该活性可保护细胞免受氧化应激，而慢性 IS 应激会损害 CuZnSOD 功能，表明对 ROS 的防御效率降低。观察到 MnSOD 活性的降低表明急性或慢性应激后 ROS 无法有效清除，这是氧化应激的特征。
