Oxidative/nitrosative stress in rats subjected to focal cerebral ischemia/reperfusion

Ischemic stroke usually initiates inflammation and oxidative/nitrosative stress leading to neuronal death.

To investigate the existence of oxidative/nitrosativestress in rats subjected to focal cerebral ischemia/reperfusion and its effects on the consequent neurological deficits.

Experimental procedures were performed on 30 adult males Wister rats. In the test group, transient focal cerebral ischemia was induced in 15 rats by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24 hours. Another 15 rats underwent the surgery at the same neck region without occlusion of CCA and served as a control group. Neurobehavioral tests were evaluated, the levels of malondialdehyde (MDA), total antioxidant capacity (TAC) and nitric oxide (NO) metabolites were measured in the serum and brain tissue to detect the effect of surgery on in each group.

The serum and brain tissue levels of MDA and NO in the test group were significantly higher compared to the control group (P < 0.001). In contrast, serum and brain tissue levels of TAC of rats subjected to ischemia reperfusion was significantly lower compared to the sham operated rats (P < 0.001). Neurological deficit of the test group correlated positively with serum TAC (CC = 0.937, P = 0.000) and brain tissue TAC (CC = 0.949, P = 0.000) and negatively with serum MDA (CC = -0.949, P = 0.000), brain tissue MDA (CC = -0.963, P = 0.000), serum NO (CC = -0.942, P = 0.000) and brain tissue NO (CC = -0.952, P = 0.000).

The study provided further evidence for the presence of oxidative/nitrosative stress in rats subjected to cerebral ischemia/reperfusion and demonstrates a relationship between oxidative/nitrosative biomarkers and the consequent neurological deficits.