Hyperglycemia-induced alterations in synaptosomal membrane fluidity and activity of membrane bound enzymes: beneficial effect of N-acetylcysteine supplementation

摘要: Diabetic encephalopathy is characterized by impaired cognitive functions that appear to underlie neuronal damage triggered glucose driven oxidative stress. Hyperglycemia-induced stress in diabetic brain may initiate structural and functional changes synaptosomal membranes. The objective of the present study was examine neuroprotective role N-acetylcysteine (NAC) hyperglycemia-induced alterations lipid composition activity membrane bound enzymes (Na(+),K(+)-ATPase Ca(2+)-ATPase) rodent model type 1 diabetes. Male Wistar rats weighing between 180 200 g were rendered a single injection streptozotocin (50 mg/kg body weight, i.p.). animals administered NAC (1.4-1.5 g/kg weight) for eight weeks along with fluidity determined. A significant increase peroxidation observed cerebral cortex rats. administration on other hand lowered near control levels. increased following chronic hyperglycemia accompanied total lipids which can be attributed levels cholesterol, triglycerides glycolipids. On contrary phospholipid ganglioside decreased. cholesterol ratio reflected decrease fluidity. Fluorescence polarization (p) DPH also confirmed influenced enzymes. An inverse correlation found fluorescence activities Na(+),K(+)-ATPase (r(2)=0.416, P<0.05) Ca(2+) ATPase (r(2)=0.604, P<0.05). significantly improve composition, restore Our results clearly suggest perturbations as major factor development encephalopathy. Furthermore, ameliorated effect thereby restoring