کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278525 | 1295823 | 2007 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A rotenone-sensitive site and H2O2 are key components of hypoxia-sensing in neonatal rat adrenomedullary chromaffin cells
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کلمات کلیدی
RLUTTXN-acetyl-l-cysteineNACAmCK+ channel - K + کانالROS - ROSOxygen-sensing - اکسیژن سنجشtetrodotoxin - تترو دوتوکسین analysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceSecretion - ترشح standard error of the mean - خطای استاندارد میانگینpostnatal day - روز پس از زایمانelectron transport chain - زنجیره انتقال الکترونLuminescence - لومینسانس SEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیMitochondria - میتوکندریاETc - و غیرهrelative light unit - واحد نسبی نورcatecholamine - کاتکولآمینهاBK channel - کانال BKReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In the perinatal period, adrenomedullary chromaffin cells (AMC) directly sense PO2 and secrete catecholamines during hypoxic stress, and this response is lost in juvenile (â¼2 week-old) chromaffin cells following postnatal innervation. Here we tested the hypothesis that a rotenone-sensitive O2-sensor and ROS are involved in the hypoxic response of AMC cultured from neonatal and juvenile rats. In whole-cell recordings, hypoxia (PO2=5-15 mm Hg) inhibited outward current in neonatal AMC; this response was reversed by exogenous H2O2 and mimicked and occluded by intracellular catalase (1000 units/ml), as well as the antioxidants, N-acetyl-l-cysteine (NAC; 50 μM) and Trolox (200 μM). Acute hypoxia decreased ROS levels and stimulated ATP secretion in these cells, as measured by luminol and luciferin-luciferase chemiluminescence, respectively. Of several mitochondrial electron transport chain (ETC) inhibitors tested, only rotenone, a complex I blocker, mimicked and occluded the effects of hypoxia on outward current, cellular ROS, and ATP secretion. Succinate donors, which act as complex II substrates, reversed the effects of hypoxia and rotenone in neonatal AMC. In contrast, in hypoxia-insensitive juvenile AMC, neither NAC nor rotenone stimulated ATP secretion though they both caused a decrease in ROS levels. We propose that O2-sensing by neonatal AMC is mediated by decreased ROS generation via a rotenone-sensitive site that is coupled to outward current inhibition and secretion. Interestingly, juvenile AMC display at least two modifications, i.e. an uncoupling of the O2-sensor from ROS regulation, and an apparent insensitivity of outward current to decreased ROS.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 145, Issue 1, 2 March 2007, Pages 130-141
Journal: Neuroscience - Volume 145, Issue 1, 2 March 2007, Pages 130-141
نویسندگان
R.J. Thompson, J. Buttigieg, M. Zhang, C.A. Nurse,