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The effect of preconditioning (PC) on the changes of nerve growth factor-induced gene A (NGFI-A) expression induced by severe hypobaric hypoxia was studied by in situ hybridization. A PC consisted of three trials of mild hypobaric hypoxia (360 Torr, 2 h) spaced at 24 h. The last trial was followed by severe hypoxia (SH; 180 Torr, 3 h) 24 h later. The PC hypoxia prevented the NGFI-A messenger RNA (mRNA) increase in the cortex, neostriatum, piriform cortex, amygdala and hippocampus detected 3 h after SH. The preconditioned SH caused a peak in NGFI-A mRNA expression at the 24 h time-point and thus abolished the dramatic decrease of the mRNA in vulnerable areas seen by 24 and 72 h after SH. The findings suggest a role of brain NGFI-A in the protective effect of hypoxic/ischemic PC. [Copyright &y& Elsevier]

Abstract: Severe hypoxia results in functional and structural injury of the brain. A preconditioning with repetitive episodes of mild hypoxia considerably ameliorates neuronal resistance to subsequent severe hypoxia. Activation of endogenous antioxidants including Cu, Zn-depending superoxide dismutase (Cu, Zn-SOD) (EC.1.15.1.1) is one of the main cell defense mechanisms against oxidative stress induced by hypoxia. Alterations of expression and enzyme activity of Cu, Zn-SOD 3 and 24h after severe hypobaric hypoxia in forebrain structures of preconditioned and non-preconditioned rats were investigated. We found that hypoxia without preconditioning suppressed the Cu, Zn-SOD enzyme activity at 3h time-point but preconditioning essentially modified the reaction to severe hypoxia by increasing the expression and activity of Cu, Zn-SOD during early stages of reoxygenation crucial for apoptosis initiation. [Copyright &y& Elsevier]

Induction of endogenous antioxidants is one of the key molecular mechanisms of cell resistance to hypoxia/ischemia. The effect of severe hypoxia on the expression of cytosolic antioxidant thioredoxin-1 (Trx) in hippocampus and neocortex was studied in preconditioned and non-preconditioned rats. The preconditioning consisted of three trials of mild hypobaric hypoxia (360Torr, 2h) spaced at 24h. Twenty-four hours after the last trial rats were subjected to severe hypobaric hypoxia (180Torr, 3h). Trx expression was studied by immunocytochemistry. In hippocampus severe hypobaric hypoxia rapidly induced Trx expression, which remained elevated still at 24h. In neocortex the enhanced expression appeared only at 24h. The preconditioning significantly augmented severe hypoxia-induced Trx-immunoreactivity at 3h but not at 24h. These findings point out that Trx contributes to mechanisms of brain tolerance to hypobaric hypoxia, especially in early periods after the exposure. [Copyright &y& Elsevier]