When rabbits acutely exposed to hypobaric
hypoxia (at imitative altitude 5,000 m, PaO2 = 6.7 kPa), the percentage of the activity of
superoxide dismutase (SOD in erythrocyte; EC 1.15.1.1) decreased respectively to 86%, 76%, 81%, 84%, 55%, 81%, 84% and 95% for a period of 0.25, 0.5, 1, 2, 3, 4, 5 and 24 h
hypoxia while MDA (
malondialdehyde) in erythrocyte and plasma increased significantly during
hypoxia periods of 1, 2, 3, 5 and 24 h (n = 5, P < 0.05, P < 0.01 vs. normoxia group). The increase of MDA in plasma could be prevented by
vitamin E (V. E, i.p, 1 mg daily for 3 consecative days before
hypoxia), but that in erythrocyte did not show significant change probably because the injected V.E. without vehicle cannot penetrate through the erythrocyte membrane effectively. The echinocytes from erythrocytes increased significantly after
hypoxia for 24 h (n = 5, P < 0.05 vs. normoxia group). However, by injecting
MPEG-SOD (monomethoxypolythlene glycol-SOD) intravenously 30 min before
hypoxia, the increase of MDA (both of erythrocyte and plasma) and echinocytes (from erythrocytes) were both inhibited obviously during
hypoxia for 24 h (n = 5, P < 0.05, P < 0.01 vs.
hypoxia group). It is inferred that the increase of MDA and echinocytes from erythrocytes may be due to lipid peroxidation by
superoxide free radicals (O2-.) generated in erythrocytes through Fenton pattern Haber-Weiss reaction during hypobaric
hypoxia.