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Regulation of Oxidant Production in Acute Lung Injury*

Karl A. Sanders, MD; T. Huecksteadt, MS; P. Xu, PhD; A. B. Sturrock, PhD; John R. Hoidal, MD
Author and Funding Information

*From the University of Utah and Salt Lake City Veterans Administration Medical Center, Salt Lake City, UT.

Correspondence to: John R. Hoidal, MD, University of Utah Medical Center, 50 N Medical Dr, Salt Lake City, UT 84124



Chest. 1999;116(suppl_1):56S-61S. doi:10.1378/chest.116.suppl_1.56S
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Extract

Free molecular oxygen probably appeared on the earth’s surface some 2 × 109 years ago as a result of photosynthetic microorganisms acquiring the ability to split water.1 It is the most abundant element in the earth’s crust, and the second most abundant element in the biosphere. Oxygen is an unusual molecule in that it has two unpaired electrons, with parallel spins. It is therefore a biradical. To overcome spin restriction, oxygen prefers to accept electrons one at a time, and the sequential addition of electrons leads to the formation of reactive oxygen intermediates (ROI), including superoxide anion (O2−), hydrogen peroxide (H2O2), hydroxyl radical (OH), and products of myeloperoxidase. ROIs are produced continuously in living cells in numerous biological processes. In rats, an average of about 1012 oxygen molecules are processed by each cell daily under basal conditions, and the leakage of partially reduced oxygen molecules is about 2%.2 Under basal conditions, human cells produce about one tenth the ROI of rats or 2 × 109 O2 and H2O2 molecules per cell per day.


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