HYPEROXIA TRIGGERS A BIPHASIC REDOX RESPONSE LEADING TO COGNITIVE IMPAIRMENT IN ADULT MICE
DOI:
https://doi.org/10.56238/arev8n5-130Keywords:
Hyperoxia, Brain, Memory, Behavior, Oxidative StressAbstract
Reactive oxygen species (ROS) are natural byproducts of aerobic metabolism, with mitochondria serving as a major source of their production. These highly reactive molecules increase during oxidative stress and brain injury. Normobaric 100% oxygen therapy is widely used to improve brain cell survival in neurological disorders; however, excessive O₂ exposure may impair antioxidant defenses, promote oxidative damage in hippocampal neurons, and contribute to cognitive deficits. Despite its clinical use, important aspects of normobaric hyperoxia remain unclear, including its therapeutic window, antioxidant response, effects on memory, and long-term consequences. This study investigated the effects of continuous exposure to 100% oxygen at normal atmospheric pressure on memory and hippocampal redox balance in adult male C57BL/6 mice. Animals were exposed to hyperoxia for 12 or 24 h, followed by evaluation of memory using the novel object recognition (NOR) test. Hippocampal superoxide dismutase (SOD) and catalase (CAT) activities, reduced glutathione (GSH), and malondialdehyde (MDA) levels were analyzed. Exposure to hyperoxia for 24 h impaired memory and increased GSH levels, whereas SOD activity and MDA levels were altered after both 12 and 24 h exposures. Overall, these findings demonstrate that 24 h of 100% oxygen exposure induces hippocampal redox imbalance, potentially contributing to neuronal damage and memory impairment.
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