8-hydroxy-2--deoxyguanosine and Movement-Disorders

The present study investigates the effects of d-allose, a rare sugar, on the inflammatory response after transient forebrain ischemia in the gerbil and whether it reduces oxidative stress (8-hydroxyl-2'-deoxyguanosine levels) and behavioral deficits.. Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 minutes. d-Allose was intraperitoneally injected immediately after ischemia (400 mg/kg). Inflammatory cytokines and oxidative damage in the hippocampus and behavioral deficits were examined 3 days after ischemia.. d-Allose administration reduced ischemia-induced cytokine production, oxidative stress, and behavioral deficits (motor and memory related).. The present results suggest that d-allose reduces brain injury after transient global ischemia by suppressing inflammation as well as by inhibiting oxidative stress.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Analysis of Variance; Animals; Blood Glucose; Blood Pressure; Cytokines; Deoxyguanosine; Disease Models, Animal; Dose-Response Relationship, Drug; Gene Expression Regulation; Gerbillinae; Glucose; Hippocampus; Male; Maze Learning; Movement Disorders; Reperfusion Injury; Sweetening Agents; Time Factors

The present study investigates the neuroprotective effects of d-allose, a rare sugar, against ischemia/reperfusion injury in a gerbil model. Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 min. D-Allose was intravenously injected before and after ischemia (200 mg/kg). Extracellular glutamate and lactate release from the gerbil brain, and PO₂ profiles were monitored during ischemia and reperfusion. We also examined neuronal death and oxidative damage in the hippocampus one week after ischemia reperfusion, and investigated functional outcome. D-Allose administration suppressed glutamate and lactate release compared to vehicle controls. Brain damage, 8-OHdG levels (a marker of oxidative stress) and locomotor activities were significantly decreased by D-allose treatment. The present results suggest that d-allose reduces delayed neuronal death and behavioral deficits after transient ischemia by changing cerebral metabolism and inhibiting oxidative stress.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Analysis of Variance; Animals; Cerebral Cortex; Deoxyguanosine; Disease Models, Animal; DNA Damage; Drug Administration Schedule; Gerbillinae; Glucose; Glutamic Acid; Ischemic Attack, Transient; Lactic Acid; Male; Microdialysis; Movement Disorders; Neurons; Oxygen; Time Factors

Oxidative stress is causally associated with the pathogenesis of Parkinson's disease (PD). Oxygen generates a large amount of reactive oxygen species (ROS). ROS including hydroxyl radicals and H(2)O(2) react with guanine residues in DNA and produce 8-hydroxydeoxyguanosine (8-OHdG). 8-OHdG serves as a biomarker for oxidative stress in various diseases.. We investigated urinary 8-OHdG levels in 61 PD patients and 28 normal subjects to evaluate the correlation with various clinical features. We quantified disease severity using the Unified Parkinson's Disease Rating Scale for motor symptoms (UPDRS part 3), the Mini-Mental State Examination (MMSE) for mental function, and the Tottori University Hallucination Rating Scale (TUHARS) for quantifying hallucinations.. There were significant correlations between 8-OHdG and all the examined parameters, but the partial correlation coefficients excluding contributions of all the other parameters showed that only TUHARS and UPDRS part 3 are significantly related to 8-OHdG. In particular, TUHARS correlates best with urinary 8-OHdG levels.. The significant correlation between urinary 8-OHdG levels and hallucinations but not with dementia suggests that hallucinations are likely to have unique but unidentified mechanisms that lead to excessive production of 8-OHdG.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Age of Onset; Aged; Aged, 80 and over; Antiparkinson Agents; Deoxyguanosine; Female; Hallucinations; Humans; Levodopa; Male; Middle Aged; Movement Disorders; Neuropsychological Tests; Oxidative Stress; Parkinson Disease; Reference Values