Selenium in ischemic stroke

Selenium plays a significant role in brain physiology, whereas data on the role of selenium in stroke pathophysiology are inconsistent. The objective of this chapter is to review current findings on the role of selenium in ischemic stroke. The existing human data demonstrate that stroke is associated with significantly reduced Se levels as well as glutathione peroxidase activity. Oppositely, we have revealed significantly higher serum Se levels in stroke, being inversely associated with brain damage markers. However, Se supplementation trials in stroke patients provided inconsistent results. Experimental studies provided a significant contribution to potential neuroprotective effects in stroke. Se supplementation was shown to increase antioxidant enzyme activity, thus reducing reactive oxygen species (ROS) production and macromolecule oxidative damage. Se-induced prevention of mitochondrial dysfunction may also significantly contribute to reduced ROS production and restoration of ATP levels. Se exposure was also shown to prevent NF-kB and AP-1 activation, thus reducing proinflammatory cytokine production and leukocyte infiltration. Reduce caspase 3 activation and apoptosis, as well as decreased autophagy, were observed under ischemic conditions in Se-treated animals. Se may also reduce adhesion molecule expression, as well as glutamate excitotoxicity, although these effects were not demonstrated in stroke models. The existing data demonstrate the neuroprotective potential of selenium in ischemic stroke. However, the majority of indications of the neuroprotective effect of selenium arise from experimental studies, whereas human data remain insufficient. Further clinical studies and especially placebo-controlled trials are strongly required to highlight the potential effects of selenium supplements in ischemic stroke management. © Springer International Publishing AG, part of Springer Nature 2018.