Introduction: Cerebral ischemia and reperfusion (I/R) are followed by the production of free radicals. The source could be NADPH oxidase isoform NOX2. Vitamin D is known to be neuroprotective.
The aim: Investigation of the effects of vitamin D pretreatment on the superoxide anion (O2·-) production, superoxide dismutase (SOD) activity, expression of NOX2 and NeuN and morphology of neurons in the hippocampus of gerbils exposed to transient global brain ischemia.
Material and methods: Gerbils were divided into seven groups: control, groups I/R1, I/R3 and I/R7 subjected to 10 minutes ischemia (ligation of both common carotid arteries) and reperfusion for 1, 3 or 7 days respectively, and groups vitD+I/R1, vitD+I/R3 and vitD+I/R7 that were pretreated with vitamin D seven days prior to corresponding I/R. Content of O2·- and SOD activity were determined by spectrophotometry. NOX2 and NeuN expression were determined by Western blot and immunohistochemistry and neuron morphology by transmission electron microscopy (TEM).
Results: The amount of O2·- in I/R1 and I/R3 groups was significantly increased. SOD activity was increased in all groups reperfused for 3 and 7 days. Expression of NOX2 was increased in I/R1 and I/R7 compared to control while in all vitamin D pretreated groups expression was decreased. Expression of NeuN was decreased after 3 days of reperfusion in all groups. Subcellular changes were seen by TEM in I/R1 group.
 Conclusion: Vitamin D regulates production of O2·- and SOD activity after I/R and ameliorates effects on the expression of NOX2. Vitamin D protects cell structure in early phases of I/R injury.

EFFECTS OF VITAMIN D PRETREATMENT ON THE NOX2, REDOX BALANCE AND NEURONAL MORPHOLOGY IN GERBILS EXPOSED TO TRANSIENT GLOBAL BRAIN ISCHEMIA