Eugenol [2-methoxy-4-(2-propenyl)phenol] prevents 6-hydroxydopamine-induced dopamine depression and lipid peroxidation inductivity in mouse striatum.

As superoxide (.O2-) and hydroxyl radical (.OH) have been implicated in the pathogenesis of Parkinson disease, free radical scavenging and antioxidants have attracted attention as way to prevent progression of this disease. We examined the effects of eugenol, an essential oil extracted from cloves, on 6-hydroxydopamine (6-OHDA)-induced dopamine (DA) reduction in the mouse striatum. Eugenol administration 3 d before and 7 more days following one intracerebroventricular 6-OHDA injection prevented the reduction of striatal DA and its metabolites. Eugenol administration for 3 d reduced the increase of thiobarbituric acid-reactive substances (an indicator of lipid peroxidation) induced by ferric ion and increased glutathione (GSH) and L-ascorbate (Asc) in the striatum. Eugenol did not change the levels of catalase, glutathione peroxidase, or superoxide dismutase-like activities. Eugenol is known to have .O2- and .OH scavenging activities in vitro. These results suggest that eugenol prevents 6-OHDA-induced DA depression by preventing lipid peroxidation directly and indirectly (via stimulation of GSH and Asc generating systems). Furthermore, increased GSH may protect cell death by conjugating with p-quinone produced in 6-OHDA auto-oxidation. The effects of eugenol treatment in this model suggest its possible usefulness for the treatment of Parkinson disease.