Oxygen poisoning of NAD biosynthesis: a proposed site of cellular oxygen toxicity.

Quinolinate phosphoribosyl transferase was rapidly inactivated in $\text{Escherichia}\text{coli}$ exposed to hyperbaric oxygen. The enzyme is essential for de novo biosynthesis of NAD in $\text{E.}\text{coli}$ 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 $\text{E.}\text{coli}$ and could be useful in cases of human oxygen poisoning.