Neurodegeneration can be caused by dysfunction of the mitochondrial electron transport chain (ETC), and thus a mitochondrial etiology has been suggested for many neurodegenerative disorders, such as Parkinson’s disease (PD), Huntington’s disease (HD), and Alzheimer’s disease (AD) (1,2). Accordingly, mitochondrial toxins have been used in animal models to mimic neurodegeneration. For example, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), via its active metabolite 1-methyl-4-phenyl-pyridinium (MPP+), selectively inhibits NADH-coenzyme Q reductase (complex I) of the ETC, and induces Parkinsonism in humans, primates, and mice (3–5). Aberrant free radical formation (4), as well as impaired mitochondrial calcium metabolism (6), have been observed to succeed ETC deficits. A cascade of events leading to cell death ensues following local infusion of MPP+, and this involves increments in superoxide radicals which in combination with nitric oxide (·NO) can yield peroxynitrite anion (ONOO−) and in turn can spontaneously decompose to produce the potentially destructive reactive hydroxyl free radicals (·OH) (7,8).