Luchese Cristiane, Pinton Simone, Nogueira Cristina W
Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil.
Pharmacol Res. 2009 Mar;59(3):194-201. doi: 10.1016/j.phrs.2008.11.006. Epub 2008 Nov 28.
Cigarette smoke exposure has been associated with oxidative stress in several organs. Antioxidant effect of diphenyl diselenide (PhSe)(2), an organoselenium compound, on oxidative damage induced by sub-chronic cigarette smoke exposure in brain and lungs of rats was investigated. Animals were exposed 5 times/week to one, two, three and four cigarettes for exposure periods of 15 min during the first, second, third and fourth weeks. Reactive species (RS) levels, enzymatic antioxidant defenses (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activities) and non-enzymatic antioxidant defenses (ascorbic acid and non-protein thiol (NPSH) levels) were examined in brain and lungs of rats. An increase in RS levels induced by cigarette smoke in both tissues of rats was demonstrated. Cigarette smoke altered enzymatic antioxidant defenses (GST, CAT and SOD activities) in both tissues, and reduced the non-enzymatic antioxidant defenses in lungs. (PhSe)(2) (0.5 mg/kg/day, 5 times/week) restored RS levels and antioxidant defenses in brain of rats exposed to cigarette smoke. (PhSe)(2) treatment increased NPSH levels, GST and GR activities per se in lungs of rats. In conclusion, sub-chronic exposure to cigarette smoke caused alterations in antioxidant defense system and a tissue-specific oxidative stress in brain and lungs of rats. (PhSe)(2) restored antioxidant defenses in lungs and brain of rats.
接触香烟烟雾已与多个器官的氧化应激相关联。研究了有机硒化合物二苯基二硒醚(PhSe)₂对大鼠脑和肺亚慢性接触香烟烟雾所致氧化损伤的抗氧化作用。动物每周接受5次暴露,在第1、2、3和4周期间分别暴露于1支、2支、3支和4支香烟,每次暴露15分钟。检测了大鼠脑和肺中的活性物质(RS)水平、酶促抗氧化防御(超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶(GR)和谷胱甘肽S-转移酶(GST)活性)以及非酶促抗氧化防御(抗坏血酸和非蛋白硫醇(NPSH)水平)。结果表明,香烟烟雾使大鼠两个组织中的RS水平升高。香烟烟雾改变了两个组织中的酶促抗氧化防御(GST、CAT和SOD活性),并降低了肺中的非酶促抗氧化防御。二苯基二硒醚(PhSe)₂(0.5毫克/千克/天,每周5次)恢复了接触香烟烟雾大鼠脑内的RS水平和抗氧化防御。二苯基二硒醚(PhSe)₂处理本身增加了大鼠肺中的NPSH水平、GST和GR活性。总之,亚慢性接触香烟烟雾导致大鼠脑和肺抗氧化防御系统改变以及组织特异性氧化应激。二苯基二硒醚(PhSe)₂恢复了大鼠肺和脑的抗氧化防御。