This study was undertaken to identify the effect of oxidative stress on the pathology of manganese intoxication through an analysis of manganese concentrations, superoxide dismutase (SOD) activities, malondialdehyde (MDA) concentrations, and the compositional changes of fatty acids from the corpus striatum of the rat brain.

Ten Sprague-Dawley rats were equally divided into two groups. Five rats in the experimental group were administered MnCl2 intraperitoneally for 4 weeks (4 mg/kg once daily, 5 days per week) and another five rats from the control group were given normal saline. Twenty-four hours after the last injection, the rats were decapitated and, the corpus striatum was isolated from the brain.

In the corpus striatums of the experimental group, manganese concentrations increased significantly by 139 % (p<0.01). The SOD activities decreased significantly by 81 % (p<0.01) and the MDA concentrations increased significantly by 138 % (p<0.01) as compared to the control group. Among fatty acids, total n-6 polyunsaturated fatty acids (PUFAs) increased significantly by 325 % (p<0.01) as compared with the control group. Arachidonic acids (AA) increased by 341 % (p<0.01), and these increases were composed mostly of n-6 polyunsaturated fatty acids (PUFA). Among n-3 PUFAs, with the exception of linolenic acids, eicosapentanoic acid (EPA) decreased significantly by 72 % (p<0.05) and docosahexanoic acids (DHA) decreased by 67 % (p<0.05) as compared with the control group.

Our results suggest that the oxygen free radicals produced by manganese may cause compositional changes of fatty acids in the corpus striatum of the rat brain. The characteristics of the fatty acids'compositional changes by manganese were a decrease of EPAs and DHAs (n-3 PUFAs), and an increase of AAs (n-6 PUFAs). These changes coupled with the decrease of SOD activity and the increase of MDA, suggest that manganese neurotoxicity is caused by lipid peroxidation mediated with oxygen free radicals, particularly superoxide radicals.