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To study the time course of oxidative damage and the molecular and cellular mechanisms underlying hypoxia-induced brain damage, some stress responses to hypoxia in rat brain, such as lactic acid(LA) and malondialdehyde (MDA) expression, superoxide dismutase (SOD) and Na+-K+-ATPase activity etc, were analysed. The role of those factors in oxidative stress was discussed too. Results showed that the SOD activity reduced obviously at 15% O2 and the level of MDA raised obviously at 12% O2, the level of lactic acid increased obviously and the Na+-K+-ATPase activity decreased obviously at 10% O2 respectively. Obviously this gave an inkling that the loss of ion homeostasis might be the result of lipid peroxidation damage. Study demonstrated that hypoxia can cause cellular lipid peroxidation, which in turn can cause inhibition/reduction in the activities of Na+-K+- ATPases. This result can, in turn, affect the intracellular concentrations of Na+,K+, alter the signal transduction pathways, and affect contractility and excitability and cellular dysfunctions such as neuropathy. Lipid peroxidation played an important role in hypoxic brain damage. Inhibition/reduction of lipid peroxidation might be available for anti-hypoxia damage.