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Effect of hypoxia and reoxygenation on the formation and release of reactive oxygen species by porcine pulmonary artery endothelial cells
Author(s) -
Yang Wenbo,
Block Edward R.
Publication year - 1995
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041640222
Subject(s) - reactive oxygen species , hyperoxia , xanthine oxidase , hypoxia (environmental) , xanthine dehydrogenase , mitochondrial ros , extracellular , intracellular , mitochondrion , pulmonary artery , chemistry , reperfusion injury , pharmacology , biology , ischemia , andrology , oxygen , biochemistry , medicine , enzyme , organic chemistry
Endothelial cells are critical targets in both hypoxia‐and reoxygenation‐mediated lung injury. Reactive O 2 species (ROS) have been implicated in the pathogenesis of hypoxic and reoxygenation lung injury, and xanthine dehydrogenase/oxidase (XDH/XO) is a major generator of the ROS. Porcine pulmonary artery endothelial cells (PAEC) have no detectable XDH/XO. This study was undertaken to examine (1) ROS production by hypoxic porcine PAEC and their mitochondria and (2) ROS production and injury in reoxygenated PAEC lacking XDH/XO activity. Intracellular H 2 O 2 generation and extracellular H 2 O 2 and O/ 2 release were measured after exposure to normoxia (room air‐5% CO 2 ), hypoxia (0% O 2 ‐95% N‐5% CO 2 ), or hypoxia followed by normoxia or hyperoxia (95% O 2 ‐5% CO 2 ). Exposure to hypoxia results in significant reductions in intracellular H 2 O 2 formation and extracellular release of H 2 O 2 and O 2 by PAEC and mitochondria. The reductions occur with as little as a 2 h exposure and progress with continued exposure. During reoxygenation, cytotoxicity was not observed, and the production of ROS by PAEC and their mitochondria never exceeded levels observed in normoxic cells. The absence of XDH/XO may prevent porcine PAEC from developing injury and increased ROS production during reoxygenation. © 1995 Wiley‐Liss, Inc.