ABSTRACT
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