Effects of lithium on oxidetive stres markers in diffuse cortical ischemia induced in rats

ConclusionWith the increase in elderly population, atherosclerosis, cerebral ischemia and vascular dementia have become more and more significant. We investigated the effects of 40mg/kg and 80mg/kg Lithium therapies in Diffuse Cerebral Cortical Ischemia and Vascular Dementia induced in Rats by bilateral Carotid artery occlusion.These are the 3 pillars of our study:1.Analysis of biochemical markers of oxidative stress in brain tissue,2.Evaluation of learning ability utilizing Morris Water Gaze (MWG) test,3.Histopathological aspects of apoptosis in hippocampal ischecmia-sensitive CA1 neurons.Biochemically studied parameteres in brain tissue (NO, GSH, SOD, CAT, MPO) were evaluated in hippocampal and cortical tissues. Oxidative parameters at the level of the cortex have shown significant differences between groups. In analysises of Hippocampal samples, GSH and NO have shown no meaningful differences, similar to cortical findings, regarding the values of GSH, SOD, CAT, and MPO, there were statistical significance amongst groups. Looking at the studied parameters, independent from dosage, lithium was associated with a decrease in cortical tissues of the oxidative stress indicator NO. Moreover, while GSH (the enzyme that plays an important role in cell protection against oxidative stress) was low in cortical tissues in dementia group compared to the control group, it increased significantly in both groups under lithium therapy. CAT, which plays an important role in the conversion of Hydrogen Peroxide to water and oxygen, and SOD, which is the primary antioxidant working against reactive oxygen species, were both increased in reaction to diffuse ischecmia in Hippocampal and cortical tissues. That increase was statistically significantly more in the group receiving lithium therapy than in the dementia group. The strng oxidant MPO enzyme increased along with the cortical diffuse ischemia, yet in the two groups receiving lithium therapy, this increase was less prominent, it was even close to the values in the control group. Litihum therapy, independant from dosage, caused a reactive increase especially in CAT and SOD, and the studied 5 parameters were also compatible with antioxident properties. Apart from the biochemical aspect, MWG test data showed an increase in learning ability in groups recieving lithium compared to the dementia group. Despite the fact that statistical comparison was not possible due to insufficient numbers, histopazthologic examination has showen that there were less apoptosis in hippocampal CA1 neurons. Our data supports the antioxidant effects of lithium againt oxidative stress in the vascular dementia model related to chronic cortical diffuse ischemia. We think lithium can have a role in the treatment of chronic cortical diffuse ischemia and vascular dementia due to its antioxident effects that we also shown in other diseases, its availability and cheap prices. However, in literature studies supporting lithiums antioxzident properties are insufficient, instead, we have data derived from studies on experimental animal models. Therefore more comprehensive study protocols are needed. This way, future therapy strategies can be developed for vascular dementia