Journal of anesthesia · 2026
Effects of a low-level superoxide-containing environment on SOD activity and cerebral ischemia-reperfusion injury.
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Uemura Keiko, Inoue Satoki, Yamanaka Kotaro, Kawaguchi Masahiko
Аннотация
PURPOSE: Superoxide (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.
METHODS: Male 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.
RESULTS: During 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.
CONCLUSION: Low-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.
METHODS: Male 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.
RESULTS: During 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.
CONCLUSION: Low-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.