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Response of liver antioxidant defense system to acute and chronic physical and psychological stresses in male rats

机译:肝脏抗氧化防御系统对雄性大鼠急慢性身心压力的反应

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摘要

The aim of this study was to evaluate the effect of acute and chronic physical and psychological stressors on the induction of oxidative stress in male rat liver. Male Wistar rats were randomly divided into 3 groups as following: control, physical and psychological stress groups. Stress was induced by communication box for one (acute), fifteen and thirty (chronic) days. Once stressor periods ended, rats were anesthetized and their liver dissected out for later assessments. Exposure to physical stress enhanced liver superoxide dismutase (SOD) (19.44 %) and glutathione S-transferase (GST) (21.84 %) activities and decreased glutathione (GSH) (30.03 %) level on the 1st day (p<0.05). SOD (24.13 and 18.43 %) and GST (27.77 and 21.27 %) activities were significantly increased, while catalase activity (29.74 and 24.41 %) and GSH level (35.05 and 31.05 %) were decreased in psychological stress group after 1 and 15 days (p<0.01 and p<0.05) compared to the 1st day value in control group, respectively. Psychological stress induced an increase in liver malondialdehyde (MDA) (46 %) and plasma corticosterone (36 %) levels on the 1st day (p<0.05). However, all parameters returned to their basal value after 30 days of stress. The results suggest that exposure to acute physical and psychological stressors induce the production of reactive oxygen species and oxidative stress in rat liver due to GSH depletion and the decreased catalase activity. The elevation of lipid peroxidation and corticosterone level in acute psychological stress may lead to more profound oxidative damage than acute physical stress. Moreover, cell protection in hepatic tissue of chronically stressed rats is indicative of possible late adaptation of the animals to stress.
机译:这项研究的目的是评估急性和慢性生理和心理应激源对雄性大鼠肝脏氧化应激的诱导作用。将雄性Wistar大鼠随机分为3组:对照组,身体和心理压力组。通讯箱持续一(急性),十五和三十(慢性)天引起压力。应激期结束后,将大鼠麻醉并解剖肝脏,以备以后评估。暴露于生理压力下可提高肝脏超氧化物歧化酶(SOD)(19.44%)和谷胱甘肽S-转移酶(GST)(21.84%)的活性,并降低谷胱甘肽(GSH)(30.03%)的水平, st (p <0.05)。 1和15天后,心理应激组的SOD(24.13和18.43%)和GST(27.77和21.27%)活性显着增加,过氧化氢酶活性(29.74和24.41%)和GSH水平(35.05和31.05%)降低( p <0.01和p <0.05)分别与对照组的第1天相比较。在第一天,心理压力导致肝脏丙二醛(MDA)(46%)和血浆皮质酮(36%)升高(p <0.05)。但是,所有参数在承受压力30天后均会恢复其基础值。结果表明,由于GSH耗竭和过氧化氢酶活性降低,暴露于急性生理和心理应激源会诱导大鼠肝脏中活性氧的产生和氧化应激。急性心理压力下脂质过氧化和皮质酮水平的升高可能导致比急性身体压力更深刻的氧化损伤。此外,慢性应激大鼠肝组织中的细胞保护表明动物可能在后期适应应激。

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