role of reduced nicotinamide adenine dinucleotide dehydrogenase activity, nitric oxide, malondialdehyde and vitamin E in Parkinson's disease

The aim of the present work was to study the role of NADH dehydrogenase enzyme [complex I] activity, nitric oxide [NO], malondialdehyde [MDA] and vitamin E [vit. E] in the etiogenesis of Parkinson's disease [PD]. This study included 20 PD patients [group I] and 20 healthy subjects [group II]. Mitochondria from platelets were isolated to detect complex I activity. Plasma nitrite and nitrate together with their platelets homogenate levels were estimated. Plasma and platelets homogenate MDA, and plasma vit. E levels were also measured. The results of the present work showed: -Significant decrease of complex I activity [n mol/min/mg protein] as compared to healthy control subjects [t=4.03, p<0.001]. -Non-significant difference between the 2 studied groups as regard plasma nitrite and nitrate and their platelets homogenate levels [micro mol/L] [P>0.05]. -Non-significant difference between the 2 groups as regard the level of MDA in both plasma [n mol/L] and platelets homogenate [n mol/mg protein] [p>0.05]. -Significant increase of plasma vit. E level [ng/ml] in group I as compared to group II [t=3.6, p<0.001]. Age, age at onset and sex of PD patients showed non-significant correlation with complex I activity, plasma nitrate, plasma and platelets MDA and plasma vit. E [p>0.05]. However, plasma nitrite levels showed significant correlation with age [r=0.467, p<0.05]. These results suggest that complex I defect is a contributing factor in the pathogenesis of PD, To be considered as a biochemical marker, it should be measured repeatedly to detect progressive decrease in activity. Nitrite, nitrate, MDA and vit. E are apparently not related to the risk for PD

Phenytoin toxicity

Of the currently treated epileptics with gr and mal and partial seizures referred to the neurology clinic and treated with phenytoin assisted by serum level monitoring, 20 patients with phenytoin toxicity have been studied. All showed a good compliance to medication, their kidney and liver functions were normal. One patient was suicidal. Five were found to suffer from organic brain disease with symptomatic epilepsy. Three were due to overdose and the other three developed the toxicity after commencement of antiepileptic polytherapy. The remaining 8 cases had the toxicity without any apparent reason. The manifestations and circumstances of toxicity were discussed