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首页> 外文期刊>Toxicological Sciences >Oxidative Stress, Inflammation, and DNA Damage in Rats after Intratracheal Instillation or Oral Exposure to Ambient Air and Wood Smoke Particulate Matter
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Oxidative Stress, Inflammation, and DNA Damage in Rats after Intratracheal Instillation or Oral Exposure to Ambient Air and Wood Smoke Particulate Matter

机译:气管内滴注或口腔暴露于环境空气和木烟颗粒物后,大鼠的氧化应激,炎症和DNA损伤

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Wood combustion is a significant source of ambient particulate matter (PM) in many regions of the world. Exposure occurs through inhalation or ingestion after deposition of wood smoke particulate matter (WSPM) on crops and food. We investigated effects of ambient PM and WSPM by intragastric or intratracheal exposure in terms of oxidative stress, inflammation, genotoxicity, and DNA repair after 24 h in liver and lung tissue of rats. Rats were exposed to WSPM from high or low oxygen combustion and ambient PM collected in areas with and without many operating wood stoves or carbon black (CB) at the dose of 0.64 mg/kg body weight. The levels of 8-oxo-7,8-dihydro-2′-deoxyguanosine, 1,N6-etheno-2′-deoxyadenosine, and 1-N2-etheno-2′-deoxyguanosine (εdG) were significantly increased with 23% (95% confidence interval [CI]: 0.1–45%), 54% (95% CI:18–90%), and 73% (95% CI: 31–134%) in the liver of rats exposed orally to CB, respectively. Rats orally exposed to PM from the wood stove area and low oxygen combustion WSPM (LOWS) had 35% (95% CI: 0.1–71%) and 45% (95% CI: 10–82%) increased levels of εdG in the liver, respectively. No significant differences were observed for bulky DNA adducts. Increased gene expression of proinflammatory cytokines, heme oxygenase-1, and oxoguanine DNA glycosylase 1 was observed in the liver following intragastric exposure and in the lung following instillation in particular of LOWS. Exposure to LOWS also increased the proportion of neutrophils in BAL fluid. These results indicate that WSPM and CB exert the strongest effect in terms of oxidative stress–induced response, inflammation, and genotoxicity in the organ closest to the port of entry.
机译:在世界许多地区,木材燃烧是环境颗粒物(PM)的重要来源。暴露是通过将木烟颗粒物(WSPM)沉积在农作物和食物上后通过吸入或摄入引起的。我们研究了大鼠肝脏和肺组织24小时后胃内或气管内暴露对环境PM和WSPM的氧化应激,炎症,遗传毒性和DNA修复的影响。大鼠在高氧燃烧或低氧燃烧下暴露于WSPM,并在有或没有许多可操作的柴火炉或炭黑(CB)的区域中以0.64 mg / kg体重的剂量收集环境PM。 8-oxo-7,8-dihydro-2'-deoxyguanosine,1,N 6 -etheno-2'-deoxyadenosine和1-N 2 -的水平etheno-2'-deoxyguanosine(εdG)显着增加,分别为23%(95%置信区间[CI]:0.1–45%),54%(95%CI:18–90%)和73%(95%CI) :31–134%)分别口服CB的大鼠肝脏。从木材炉灶区域和低氧燃烧WSPM(LOWS)口服暴露于PM的大鼠的sdG水平升高了35%(95%CI:0.1–71%)和45%(95%CI:10–82%)。肝分别。对于大的DNA加合物没有观察到显着差异。观察到胃内暴露后肝脏中和滴注后尤其是LOWS后肺中促炎性细胞因子,血红素加氧酶-1和氧鸟嘌呤DNA糖基化酶1的基因表达增加。暴露于LOWS也会增加BAL液中嗜中性粒细胞的比例。这些结果表明,WSPM和CB在氧化应激诱导的反应,炎症和最接近进入口的器官的遗传毒性方面发挥最强的作用。

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