The effect hyperhomocsteinemia on nöronal and glial markers in rat brain.

T.CFIRAT ÜNIVERSITESISAĞLIK BILIMLERI ENSTITÜSÜTIP FAKÜLTESİ FİZYOLOJİ ANABİLİMDALITHE EFFECT OF HYPERHOMOCYSTEINEMIO ON NOROAL AND GLIALMARKERS IN RAT BRAINMehmet ÖZERDanışmanProf. Dr. Gıyassettin BAYDAŞABSTRACTHomocysteine; is an amino acid with a sulphure-containing methionin. One of themajor effects of homocystein is to provacate the oksidan stres and reduce deffence of thebody. Research showed that injection of homocystein induces the free radicals production inbrain tisue and leads to lipid peroxidation. There are few information about the relationbetween the brain disfonction and hyperhomocysteinemia. Reseaches mentioned that totalplasma homocystein level is a suitable symptom to show the decrase of cofactor level intissues and to eveluate the cognitive performance of old people. Increases in homocysteinelevels leads to inhibition of neuronal cell proliferation, increase in Ca concentrstion induceapopotasis by pragmestation of DNA . Furthermore, homocystein causes neurotoxicity byover stimulation of glutamat receptors, snaptic dysfunction and inhibits neuronal energymetabolism.The aim of this investigale was to study the effects of high level of homocysteine onneuronal toxicity, neuronal plasticity and cognitive performans glial marker S100B andGFAP in hyppocampus and cortex by using western blot on the levels of methods.İn adtitioneffects of homocystein on the level of lypid peroxidation (LOP) and Glutation (GSH) .Protective effects ofmelatonin againt hyperhomocysteinemin were studied as well.For this purpose the level of S100B, GFAP, MDA and GSH mesured in hyppocampusand cortex of control group, homocystein and melatonin given rats. The differences betweengroups were measured by using ANOVA. For Post-Hoc estimation t-test of Bonferroniıs testwas used. P value was accepted as <0.05 and the lower value from <0.005 was accepted assignificant.There was, a significant increase in GFAP contents of hyppocampus and cortex ofhomocystein group comparing with contrrol (P<0.001). Administration of melatoninprevented the increase in the levels of GFAP level (P<0.05). A significant increase in S100Blevel in cortex of homocystein groups was faund comparing with contrrol group (P<0.001).But there was no significant increase in S100B protein level in hyppocampus of homocysteinfaund (P>0.05). Administation of melathonin prevented the increase in theleves of S100B(P<0.01) induced by hypohomocystenemia.There was no difference between NSE levels in control, to and homosistein+to groups.During this study we found that gial markers increase with LPO increasing of level. Glialreactivity occurs due to oxidant stress because of homosterin exposure. Homosistein increaseLPO level and decrease antioxidant enzyme levels in tissues and plasma. However, melatonindecrease LPO level and increase antioxidant enzyme levels in tissues and plasma.Key Words: Homocystein, hippocampus, cortex, S100B, GFAB, NSE, melatonin