{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T16:21:41Z","timestamp":1785860501842,"version":"3.56.0"},"reference-count":82,"publisher":"SAGE Publications","issue":"9","license":[{"start":{"date-parts":[[2018,4,9]],"date-time":"2018-04-09T00:00:00Z","timestamp":1523232000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2019,9]]},"abstract":"<jats:p>\n                    Mortality from perinatal hypoxic\u2013ischemic (HI) brain injury reached 1.15 million worldwide in 2010 and is also a major factor for neurological disability in infants. HI directly influences the oxidative phosphorylation enzyme complexes in mitochondria, but the exact mechanism of HI-reoxygenation response in brain remains largely unresolved. After induction of HI-reoxygenation in postnatal day 10 rats, activities of mitochondrial respiratory chain enzymes were analysed and complexome profiling was performed. The effect of conformational state (active\/deactive (A\/D) transition) of mitochondrial complex I on H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    release was measured simultaneously with mitochondrial oxygen consumption. In contrast to cytochrome c oxidase and succinate dehydrogenase, HI-reoxygenation resulted in inhibition of mitochondrial complex I at 4\u2009h after reoxygenation. Immediately after HI, we observed a robust increase in the content of deactive (D) form of complex I. The D-form is less active in reactive oxygen species (ROS) production via reversed electron transfer, indicating the key role of the deactivation of complex I in ischemia\/reoxygenation. We describe a novel mechanism of mitochondrial response to ischemia in the immature brain. HI induced a deactivation of complex I in order to reduce ROS production following reoxygenation. Delayed activation of complex I represents a novel mitochondrial target for pathological-activated therapy.\n                  <\/jats:p>","DOI":"10.1177\/0271678x18770331","type":"journal-article","created":{"date-parts":[[2018,4,9]],"date-time":"2018-04-09T07:46:50Z","timestamp":1523260010000},"page":"1790-1802","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":31,"title":["Deactivation of mitochondrial complex I after hypoxia\u2013ischemia in the immature brain"],"prefix":"10.1177","volume":"39","author":[{"given":"Anna","family":"Stepanova","sequence":"first","affiliation":[{"name":"School of Biological Sciences, Queen's University Belfast, Medical Biology Centre, Belfast, UK"},{"name":"Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Csaba","family":"Konrad","sequence":"additional","affiliation":[{"name":"Feil 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