Polyamines, DNA synthesis, and tolerance to hyperoxia of mice and rats.

Adaptation to hyperoxia has been attributed to increased activities of protective enzymes, but we suggest that an additional factor may be the lung's capacity to repair itself in hyperoxia. Such repair would require increased polyamines, but there are reports that two key enzymes of polyamine metabolism are suppressed by hyperoxia or oxidants. Because rats can adapt to hyperoxia but mice cannot, we compared their changes of polyamine metabolism and judged cell repair by using [3H]thymidine to estimate DNA synthesis. Both species developed increased ornithine decarboxylase activity and putrescine content, but the mouse did not develop increased S-adenosylmethionine decarboxylase activities or increases of spermidine and spermine as did the rat when exposed to 85% O2. Furthermore, we confirmed that the rat lung does respond to hyperoxia with increased DNA synthesis, but the mouse lung does not. The results suggest that in addition to increased activities of protective enzymes, increased repair processes in the rat lung may play a role in its capacity to adapt to hyperoxia. The incomplete response of polyamine metabolism in mice may contribute to their inability to adapt in hyperoxia.