Filipović Dragana, Pajović Snezana B
Laboratory of Molecular Biology and Endocrinology, Institute of Nuclear Sciences Vinca, P. O. Box 522-090, 11000, Belgrade, Serbia.
Cell Mol Neurobiol. 2009 Jul;29(5):673-81. doi: 10.1007/s10571-009-9375-5. Epub 2009 Mar 13.
Neuroendocrine stress (NES) causes increase of glucocorticoids and alters physiological levels of reactive oxygen species production in cells, which might involve modifications in the antioxidant defense system. We investigated the hypothesis that acute, chronic, or combined stress alters copper-zinc superoxide dismutase (CuZnSOD) expression pattern at both, mRNA and subcellular protein level in the cerebral cortex and hippocampus of rats and that there may be a relationship between stress-induced corticosterone and CuZnSOD expression. The most effective stress model which led to the most pronounced changes in CuZnSOD expression patterns was also investigated. Our results demonstrated that acute stress immobilization up-regulates mRNA expression of hippocampal CuZnSOD, while cytosolic protein expression of this enzyme was increased in both brain structures. Chronic stress isolation had no effect on either mRNA and protein expression level and caused a lack of significant up-regulation to a novel acute stressors. The presence of this protein in nuclear fractions of both brain structures was also confirmed. The elevated cytosolic CuZnSOD protein levels following acute immobilization might reflect on the defense system against oxidative stress. Chronic isolation compromises CuZnSOD protein expression, which may lead to the inefficient defense against reactive oxygen species (ROS). The stress-triggered CuZnSOD protein expression was not correlated by the corresponding mRNA. The results suggest that different stress models exert a different degree of influence on mRNA and protein level of CuZnSOD in both brain structures as well as serum corticosterone.
神经内分泌应激（NES）会导致糖皮质激素增加，并改变细胞内活性氧产生的生理水平，这可能涉及抗氧化防御系统的改变。我们研究了以下假设：急性、慢性或联合应激会改变大鼠大脑皮层和海马中铜锌超氧化物歧化酶（CuZnSOD）在mRNA和亚细胞蛋白水平的表达模式，并且应激诱导的皮质酮与CuZnSOD表达之间可能存在关联。我们还研究了导致CuZnSOD表达模式最显著变化的最有效应激模型。我们的结果表明，急性应激固定会上调海马中CuZnSOD的mRNA表达，而该酶的胞质蛋白表达在两个脑区均增加。慢性应激隔离对mRNA和蛋白表达水平均无影响，并且对新的急性应激源缺乏显著的上调作用。同时也证实了该蛋白在两个脑区的核部分中的存在。急性固定后胞质CuZnSOD蛋白水平升高可能反映了对抗氧化应激的防御系统。慢性隔离会损害CuZnSOD蛋白表达，这可能导致对活性氧（ROS）的防御效率低下。应激触发的CuZnSOD蛋白表达与相应的mRNA不相关。结果表明，不同的应激模型对两个脑区中CuZnSOD的mRNA和蛋白水平以及血清皮质酮施加不同程度的影响。
