The Effect of Tetrahydroisoquinoline on the Mitochondrial Respiration
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism has been considered as the best model available at present of Parkinson’s disease (1–4). The neurotoxic effect of MPTP on the nigrostriatal dopaminergic neurons resides in the inhibition of the mitochondrial respiration by 1-methyl-4-phenylpyridinium ion (MPP+), an oxidation product of MPTP, resulting in the energy crisis of those neurons (5–11). Since the discovery of MPTP and MPP+, it has been proposed that (an) exogenous or (an) endogenous MPTP-like substance(s) may be the cause of Parkinson’s disease. 1,2,3,4-Tetrahydroisoquinoline (TIQ) has emerged as one of such candidates (12). TIQ was shown to inhibit the state 3 respiration of the mitochondria (13). This effect of TIQ on the mitochondrial respiration is similar to that of MPP+. In this communication, we report effects of TIQ on the enzyme-protein complexes in the electron transport system and on the respiratory enzymes in the tricarboxylic acid (TCA) cycle.
KeywordsTyrosine Hydroxylase Mitochondrial Respiration Tricarboxylic Acid Malate Dehydrogenase Electron Transport System
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