Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the effect of various compounds, known as antioxidants, on the level of hyperoxia (80-90% O2)-induced chromosomal aberrations in Chinese hamster ovary cells: ascorbic acid, alpha-tocopherol, carnosine, imidazole-4-acetic acid, glutathione monoethylester, N-acetylcysteine and ethoxyquin. Carnosine (beta-alanyl-histidine) appeared to be the only compound that reduced chromosomal breakage. The effect was also present in cultures post-treated with caffeine (at 2.5 mM, 3 h before harvest), indicating that the apparent protection was not due to selective arrest of chromosomally damaged cells in the G2 phase of the cell cycle. Imidazole-4-acetic acid, a compound structurally very similar to carnosine, had no detectable effect. Ascorbic acid, N-acetylcysteine, glutathione monoethylester and ethoxyquin were found to have a pro-oxidant effect, i.e. they apparently potentiated the clastogenic effect of hyperoxia. Carnosine is the first compound shown to protect against the clastogenicity of normobaric hyperoxia and may thus be a useful tool in elucidating the underlying mechanism.
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PMID:Effect of antioxidants on hyperoxia-induced chromosomal breakage in Chinese hamster ovary cells: protection by carnosine. 194 22

This study investigated whether increased muscle acetylcarnitine provision (acetate infusion) or hyperoxia (100% O(2)) would increase the rate of oxidative phosphorylation and reduce the reliance on muscle substrate phosphorylation after the onset of moderate exercise. Eight subjects completed three randomized trials, each separated by 1 wk: 1) saline infusion for 1 h before exercise, while breathing room air for 20 min before exercise and during 120 s of cycling at 65% maximal exercise (VO(2 max)) (CON), 2) saline infusion with 4 mmol/kg body wt sodium acetate, while breathing room air before and during exercise (ACE), and 3) saline infusion and breathing 100% O(2) before and during exercise (HYP). Muscle biopsies were sampled at rest and after 30 and 120 s of exercise. ACE increased muscle acetyl-CoA and acetylcarnitine contents at rest vs. CON and HYP [22.9 +/- 2.8 vs. 8.9 +/- 2.4 and 10.5 +/- 1.8 micromol/kg dry muscle (dm); 11.0 +/- 1.2 vs. 3.5 +/- 1.3 and 4.0 +/- 1.2 mmol/kg dm]. Acetate had no effect on resting pyruvate dehydrogenase activity in the active form (PDH(a)) among CON, ACE, and HYP. During exercise, acetyl-CoA and acetylcarnitine were unchanged in ACE but increased over time in the CON and HYP trials, and PDH(a) increased similarly in all trials. Muscle phosphocreatine use, lactate accumulation, and substrate phosphorylation energy provision after 30 or 120 s of exercise were similar in all trials. In summary, increased acetylcarnitine availability did not accelerate the rate of oxidative phosphorylation at the onset of exercise, suggesting that this is not a site of extra substrate. Hyperoxia had no effect on substrate phosphorylation, suggesting that O(2) availability does not limit oxidative phosphorylation at the onset of moderate exercise.
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PMID:Effects of acetate infusion and hyperoxia on muscle substrate phosphorylation after onset of moderate exercise. 1170 27