Mechanisms of Oxygen Toxicity at the Cellular Level.
Abstract
Significant progress occurred in four areas: (1) Effect of hyperoxia on reverse glycolysis: We concluded that glucose protects Escherichia coli against hyperoxia better than other intermediates later in glycolysis and in the Krebs cycle but not because of a specific inhibition of reverse glycolysis. There was no significant impairment of the three enzymes of reverse glycolysis: fructose-1,6-diphosphatase, phosphoenolpyruvate synthase, or phosphoenolpyruvate carboxykinase. (2) Effect of hyperoxia on synthesis of RNA, DNA and pyridine nucleotide coenzymes: Evidence was obtained for direct inhibition of RNA synthesis in cells poisoned by hyperoxia, while protein synthesis was not directly affected. DNA synthesis is impaired but it is not proven whether this is direct or indirect. NAD and NADH were severly decreased in cells during poisoning by hyperoxia. This decrease was prevented by niacin, but not quinolinate which is consistent with poisoning of quinolinate phosphoribosyltransferase (QPT), as previously reported. PRPP does not protect against oxygen poisoning, PRPP synthetase is not affected by hyperoxia, but PRPP accumulates in oxygen poisoned cells which is in agreement with inhibiton of QPT. (3) Relationship of thiamine to oxygen toxicity.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 30, 1980
- Accession Number
- ADA087831
Entities
People
- Olen R. Brown