Oxygen poisoning of NAD biosynthesis: a proposed site of cellular oxygen toxicity. |
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Authors: | O Brown F Yein D Boehme L Foudin C S Song |
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Affiliation: | 1. The John M. Dalton Research Center, University of Missouri-Columbia, Missouri 65211 USA;2. Department of Veterinary Microbiology, University of Missouri-Columbia, Missouri 65211 USA |
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Abstract: | Quinolinate phosphoribosyl transferase was rapidly inactivated in exposed to hyperbaric oxygen. The enzyme is essential for de novo biosynthesis of NAD in and man. Because of its sensitivity and essentiality, inactivation of this enzyme is proposed as a significant mechanism of cellular oxygen toxicity. Niacin which enters the NAD biosynthetic pathway below the oxygen-poisoned enzyme provided significant protection against the decrease in pyridine nucleotides and the growth inhibition from hyperoxia in and could be useful in cases of human oxygen poisoning. |
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