The
neuroprotective effects of synthesized lipophylic
antioxidant from hindered
phenol class (U-18) and hydrophylic antioxidative
enzyme superoxide dismutase (SOD) were tested on long-term mouse hippocampal cell cultures exposed to
hypoxia/reoxygenation. The application of
U-18 to the cultures during 6-8 hr
hypoxia followed by 16-18 hr reoxygenation in the absence of
antioxidant significantly reduced neuronal death. Thus, lipophylic
free radical scavenger may exert a delayed
neuroprotective effect, probably owing to persistent incorporation into
phospholipid membranes and prevention of their lipid peroxidation by means of prolonged intramembranous
free radical quenching. On the other hand, the exposure of the cultures to
U-18 during 15 hr
hypoxia without subsequent reoxygenation also led to significant reduction of neuronal death compared with that observed without
antioxidant. These findings suggest that
free radical neuronal damage may occur under conditions of prolonged restricted
oxygen access to the neurons. The hypoxic/posthypoxic neuronal injury significantly decreased in the cultures exposed to hydrophylic cytoplasmic
enzyme SOD (300 U/ml). The
neuroprotective effects of both lipophylic
U-18 and hydrophylic SOD on the cultures exposed to
hypoxia/reoxygenation might reflect the damaging
free radical overproduction in different morphofunctional compartments of the nerve cell.