ArticleJournal of anesthesia2026
Effects of a low-level superoxide-containing environment on SOD activity and cerebral ischemia-reperfusion injury.
Article in Journal of anesthesia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Funding
Abstract
purposeSuperoxide (SO), a cause of ischemia-reperfusion injury, damages tissues. Superoxide dismutase (SOD) acts as a defense mechanism against SO but is also affected by SO itself. We hypothesized that exposure to a low-level superoxide-containing environment (hereafter referred to as "low-level SO exposure") activates SOD and may influence the response to transient forebrain ischemia. This study investigated changes in hippocampal SOD activity with low-level SO exposure and in relation to transient forebrain ischemia.
methodsMale Sprague-Dawley rats were used. SOD activity was measured in rats with low-level SO exposure. Transient forebrain ischemia was induced, and SOD activity was measured before and after ischemia. Neurological and histological evaluations were performed.
resultsDuring low-level SO exposure, SOD activity did not change significantly, but increased significantly at 3 days after cessation of exposure and was significantly suppressed at 7 days. Post-ischemic SOD activity in rats without low-level SO exposure was significantly higher than in normal rats. Rats with low-level SO exposure before ischemia showed significantly lower SOD activities than rats without low-level SO exposure. No significant differences were observed in neurological or histological outcomes. Post-ischemia low-level SO exposure did not affect SOD activity or outcomes.
conclusionLow-level SO exposure temporarily increased SOD activity after cessation of exposure but suppressed it 7 days later. Pre-ischemia low-level SO exposure reduced post-ischemic SOD activity, but did not affect neurological or histological outcomes. These findings suggest that changes in SOD activity induced by low-level SO exposure may not be sufficient to influence ischemia-reperfusion injury.
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