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Systemic hypoxia lead to deplete amount of ATP in tissues that is caused by inefficiency of ATP production in anaerobic glycolysis. Furthermore, degradation of ATP will activate xanthine oxidase activity, that has side effect free radical production and oxidative stress. In addition, hypoxia is known lead to HIF-1 stabilities by reducing prolyl hydroxylase activity and renin expression. Higher renin expression can cause hypertension. This research aim is to reveal how strong oxidative stress damages of systemic hypoxia (MDA) correlated to HIF-1 and renin expression in kidney tissue. This experimental study conducted using rats induced by hypoxic states for 1 day, 3 days, 7 days, and 14 days with gas mix 10% O2, 90% N2 to proof systemic hypoxia, produce free radical damaged (malondialdehyde/MDA), increase expression of HIF-1 and renin mRNA relative expression. MDA was measured by spectrophotometric method, HIF-1 by Immunohysto chemistry, and renin mRNA using RT-PCR. Results showed that in systemic hypoxia MDA were increased significantly in 7 and 14 days of hypoxia, but in 14days MDA level was lower than 7 days hypoxia. HIF-1 increased during hypoxia. Relative expression of renin mRNA was increased during systemic hypoxia and the peak was at 3day hypoxia. MDA has strong correlation to HIF-1 than to renin mRNA relative expression. We conclude that MDA as product of membrane damage caused by free radicals has strong correlation to HIF-1α in systemic hypoxia. Key word: Malondialdehyde, renin mRNA, HIF-1alpha, hypoxia, oxidative stress

Hypoxia increased malondialdehyde from membrane damages is highly correlated to HIF-1α but not to renin expression in rat kidney