OXYGEN POISONING OF NAD BIOSYNTHESIS - PROPOSED SITE OF CELLULAR OXYGEN-TOXICITY

Quinolinate phosphoribosyl transferase was rapidly inactivated in Escherichia coli exposed to hyperbaric O2. The enzyme is essential for de novo biosynthesis of NAD in E. coli and man. Because of its sensitivity and essentiality, inactivation of this enzyme is proposed as a significant mechanism of cellular O2 toxicity. Niacin which enters the NAD biosynthetic pathway below the O2-poisoned enzyme provided significant protection against the decrease in pyridine nucleotides and the growth inhibition from hyperoxia in E. coli and could be useful in cases of human O2 poisoning.