کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8271164 | 1534981 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Developmental differences in hyperoxia-induced oxidative stress and cellular responses in the murine lung
ترجمه فارسی عنوان
اختلالات رشدی در استرس اکسیداتیو ناشی از هیپوکسی و پاسخ سلولی در ریه های موش صحرایی
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کلمات کلیدی
BPDAECAT2NOX1AOEPASMCNADPH oxidase 1 - NADPH اکسیداز 1ROS - ROSAntioxidant enzyme - آنزیم آنتی اکسیدانmitochondrial oxidative stress - استرس اکسیداتیو میتوکندریDevelopmental differences - تفاوت های رشدLung development - توسعه ریهBronchopulmonary dysplasia - دیسپلازی ریویFree radicals - رادیکال آزادpostnatal day - روز پس از زایمانPulmonary artery smooth muscle cell - سلول عضله صحی عروق ریویalveolar epithelial cell - سلول های اپیتلیال آلوئولارlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Exposure of newborn mice to high inspired oxygen elicits a distinct phenotype of compromised alveolar and vascular development, although lethality during long-term exposure is lower in newborns compared to adults. As the effects of hyperoxia are mediated by excessive reactive oxygen species (ROS) generation, we hypothesized that newborn mice may exhibit enhanced expression of antioxidant defenses or attenuated ROS generation compared with adults. We measured subcellular oxidant responses to acute hyperoxia in lung slices and alveolar epithelial cells at varying time points during postnatal murine lung development. Oxidant stress was assessed using RoGFP, a ratiometric protein thiol redox sensor, targeted to the cytosol or the mitochondrial matrix. In contrast to newborn resistance to oxygen-induced mortality, cells of lung slices from younger mice demonstrated exaggerated mitochondrial matrix oxidant stress compared to adults, whereas oxidant stress responses in the cytosol were absent. Cell death in lung slices from newborn mice exposed to 48Â h of hyperoxia was also greater than for adults. Consistent with these findings, expression of antioxidant enzymes in newborn lungs was lower than in adults, and induction of antioxidant levels and activity during 24Â h of in vivo exposure was absent. However, expression of the reactive oxygen species-generating enzyme NADPH oxidase 1 was increased with hyperoxic exposure in the young but not the adult lung. Collectively, these results suggest that the greater lethality in adult animals may be more likely attributed to processes such as inflammation than to differences in antioxidant defenses. Therapies for neonatal and adult oxidative lung injury should therefore consider and address developmental differences in oxidative stress responses.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 61, August 2013, Pages 51-60
Journal: Free Radical Biology and Medicine - Volume 61, August 2013, Pages 51-60
نویسندگان
Sara K. Berkelhamer, Gina A. Kim, Josiah E. Radder, Stephen Wedgwood, Lyubov Czech, Robin H. Steinhorn, Paul T. Schumacker,