| Abstract: | The toxic effects of high pressure oxygen on the isolated toad urinary bladder have been studied. Sodium transport in this system is reversibly inhibited by high pressure O2. This inhibition is potentiated by adrenal steroid hormones, and occurs despite both increased glycolytic and Kreb's cycle flux and tissue ATP content. High pressure O2 leads to increased pyruvate/lactate and pyruvate/malate redox couples, as well as to a decrease in the weight percentage of phospholipid long-chain unsaturated fatty acids and [2-14C]pyruvate incorporation into tissue lipid. During recovery from high pressure O2 treatment, [2-14C]Pyruvate incorporation into lipid is increased and the weight percentage of long-chain unsaturated fatty acids increases. These data indicate that high pressure O2 poisoning in this tissue does not result from an inhibition of carbohydrate metabolism, but may result from the formation of toxic lipid peroxides. |
