Torres R L, Torres I L S, Gamaro G D, Fontella F U, Silveira P P, Moreira J S R, Lacerda M, Amoretti J R, Rech D, Dalmaz C, Belló A A
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 90035-003 Porto Alegre, RS, Brasil.
Braz J Med Biol Res. 2004 Feb;37(2):185-92. doi: 10.1590/s0100-879x2004000200004. Epub 2004 Jan 30.
Exposure to stress induces a cluster of physiological and behavioral changes in an effort to maintain the homeostasis of the organism. Long-term exposure to stress, however, has detrimental effects on several cell functions such as the impairment of antioxidant defenses leading to oxidative damage. Oxidative stress is a central feature of many diseases. The lungs are particularly susceptible to lesions by free radicals and pulmonary antioxidant defenses are extensively distributed and include both enzymatic and non-enzymatic systems. The aim of the present study was to determine lipid peroxidation and total radical-trapping potential (TRAP) changes in lungs of rats submitted to different models of chronic stress. Adult male Wistar rats weighing 180-230 g were submitted to different stressors (variable stress, N = 7) or repeated restraint stress for 15 (N = 10) or 40 days (N = 6) and compared to control groups (N = 10 each). Lipid peroxidation levels were assessed by thiobarbituric acid reactive substances (TBARS), and TRAP was measured by the decrease in luminescence using the 2-2'-azo-bis(2-amidinopropane)-luminol system. Chronic variable stress induced a 51% increase in oxidative stress in lungs (control group: 0.037 +/- 0.002; variable stress: 0.056 +/- 0.007, P < 0.01). No difference in TBARS was observed after chronic restraint stress, but a significant 57% increase in TRAP was presented by the group repeatedly restrained for 15 days (control group: 2.48 +/- 0.42; stressed: 3.65 +/- 0.16, P < 0.05). We conclude that different stressors induce different effects on the oxidative status of the organism.
暴露于应激源会引发一系列生理和行为变化,以维持机体的内稳态。然而,长期暴露于应激源会对多种细胞功能产生有害影响,比如抗氧化防御受损导致氧化损伤。氧化应激是许多疾病的核心特征。肺对自由基损伤尤为敏感,肺部抗氧化防御广泛分布,包括酶促和非酶促系统。本研究的目的是确定不同慢性应激模型下大鼠肺组织中脂质过氧化和总自由基捕获能力(TRAP)的变化。体重180 - 230克的成年雄性Wistar大鼠接受不同应激源处理(可变应激,N = 7)或重复束缚应激15天(N = 10)或40天(N = 6),并与对照组(每组N = 10)进行比较。脂质过氧化水平通过硫代巴比妥酸反应性物质(TBARS)评估,TRAP通过使用2 - 2'-偶氮双(2 - 脒基丙烷)-鲁米诺系统的发光减少来测量。慢性可变应激导致肺组织氧化应激增加51%(对照组:0.037±0.002;可变应激组:0.056±0.007,P < 0.01)。慢性束缚应激后未观察到TBARS有差异,但重复束缚15天的组TRAP显著增加57%(对照组:2.48±0.42;应激组:3.65±0.16,P < 0.05)。我们得出结论,不同应激源对机体氧化状态产生不同影响。