Sulfur dioxide reduces hippocampal cell death and improves learning and memory deficits in a rat model of transient global ischemia/reperfusion

OBJECTIVE(S): According to recent the findings, sulfur dioxide (SO(2)) is produced by the cardiovascular system, influencing some major biological processes. Based on previous research, SO(2) exhibits antioxidant effects and inhibits apoptosis following cardiac ischemia/reperfusion. Therefore, the objective of the current study was to examine the neuroprotective impact of SO2 following global cerebral ischemia/reperfusion (I/R). MATERIALS AND METHODS: Forty-eight male Wistar rats that weighed 260–300 g, were randomly allocated into 4 groups: sham group (n=12), I/R group (n=12), and I/R+SO(2) groups (NaHSO(3 )and Na(2)SO(3); 1:3 ratio; 5 and 10 µg/kg, respectively; for 3 days, n=12). Cerebral ischemia model was prepared by occlusion of both common carotid arteries for 20 min. Saline as a vehicle and SO(2) donor at doses 5 µg/kg (intraperitoneally) were injected for 3 days after reperfusion. Four days after ischemia, the passive avoidance memory test was carried out in four groups, and after behavioral assessment, necrosis, apoptosis, and antioxidant enzyme analysis were carried out. RESULTS: O(2) treatment could significantly improve memory impairments in rats with cerebral ischemia/reperfusion (I/R) (P<0.05). An increase in both superoxide dismutase and glutathione and a reduction in malondialdehyde were reported in the SO(2) group versus the ischemic group (P<0.05). Moreover, SO(2) could significantly decrease necrotic and apoptotic cells in the CA1 region (P<0.01). CONCLUSION: According to the findings, SO(2) exerts significant neuroprotective effects on cerebral I/R due to its antioxidant activity.