{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T02:34:37Z","timestamp":1788489277077,"version":"build-2803163510"},"reference-count":28,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[2015,1,1]]},"abstract":"<jats:p> Reactive oxygen species (ROS) mainly originating from NADPH oxidases have been shown to be involved in the carotid body (CB) oxygen-sensing cascade. For measuring ROS kinetics, type I cells of the mouse CB in an ex vivo preparation were transfected with the ROS sensor construct FRET-HSP33. After 2 days of tissue culture, type I cells expressed FRET-HSP33 as shown by immunohistochemistry. In one population of CBs, 5 min of hypoxia induced a significant and reversible decrease of type I cell ROS levels ( n = 9 CBs; P &lt; 0.015), which could be inhibited by 4-(2-aminoethyl)benzensulfonylfluorid (AEBSF), a highly specific inhibitor of the NADPH oxidase subunits p47<jats:sub>phox<\/jats:sub> and p67<jats:sub>phox<\/jats:sub>. In another population of CBs, however, 5 min of hypoxia induced a significant and reversible increase of ROS levels in type I cells ( n = 8 CBs; P &lt; 0.05), which was slightly enhanced by administration of 3 mM AEBSF. These different ROS kinetics seemed to coincide with different mice breeding conditions. Type I cells of both populations showed a typical hypoxia-induced membrane potential (MP) depolarization, which could be inhibited by 3 mM AEBSF. ROS and MP closely followed the hypoxic decrease in CB tissue oxygen as measured with an O<jats:sub>2<\/jats:sub>-sensitive dye. We conclude that attenuated p47<jats:sub>phox<\/jats:sub> subunit activity of the NADPH oxidase under hypoxia is the physiological trigger for type I cell MP depolarization probably due to ROS decrease, whereas the observed ROS increase has no influence on type I cell MP kinetics under hypoxia. <\/jats:p>","DOI":"10.1152\/ajpcell.00370.2013","type":"journal-article","created":{"date-parts":[[2014,10,16]],"date-time":"2014-10-16T01:28:54Z","timestamp":1413422934000},"page":"C61-C67","source":"Crossref","is-referenced-by-count":14,"title":["Type I cell ROS kinetics under hypoxia in the intact mouse carotid body ex vivo: a FRET-based study"],"prefix":"10.1152","volume":"308","author":[{"given":"A.","family":"Bernardini","sequence":"first","affiliation":[{"name":"Institute of Physiology, University of Duisburg-Essen, Essen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U.","family":"Brockmeier","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Duisburg-Essen, Essen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Metzen","sequence":"additional","affiliation":[{"name":"Institute of Physiology, University of Duisburg-Essen, Essen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"U.","family":"Berchner-Pfannschmidt","sequence":"additional","affiliation":[{"name":"Department of Ophthalmology, University of Duisburg-Essen, Essen, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E.","family":"Harde","sequence":"additional","affiliation":[{"name":"Institute for Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences, Goethe University, Frankfurt, Germany; 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