An irreversible inhibitor of complex II in the mitochondria, 3-nitropropionic acid (3-NP), induces bilateral striatal lesions with many neuropathological features of Huntington’s disease (HD) in rats. It is widely used as a model of HD. Chronic systemic treatment of 3-NP for 4 days in rats (10, 15 and 20 mg/kg) caused a significant dose-dependent reduction in succinate dehydrogenase activity, which was evident in histochemical as well as in biochemical assays. Splayed toes, and moderate to severe immobility in the hind limbs marked 3-NP administration in adult rats. A dose-dependent rise in striatal dopamine level, as measured employing HPLC-electrochemistry, was also evident. The rise in dopamine level was consistent in adult (4-6 months), but inconsistent in younger rats (2-3 months). A significant rise in NADH:ubiquinone reductase activity was indicated in the mitochondrial fractions prepared from the cerebral cortex region of rats treated with 3-NP. This was equally visible in the rotenone sensitive and insensitive fractions of the enzyme. Our results strongly suggest involvement of Complex I dysfunction in the behavioral and dopaminergic aberrations as seen in HD.