Elsevier

Biochemical Pharmacology

Volume 37, Issue 23, 1 December 1988, Pages 4573-4574
Biochemical Pharmacology

Short communication
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and free radicals in vitro

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    To confirm that loss of NTH-1 reduced vulnerability of DA neurons to chemically induced damage and decreased viability, we measured survival of DA neurons in the absence or presence of the dopamine analog 6-hydroxy dopamine (6-OHDA) or the mitochondrial poison 1-methyl-4-phenylpyridinium (MPP+). Both of these neurotoxins generate ROS by inhibiting flux through the mitochondrial electron transport chain, resulting in ROS-induced neuronal loss (Hernandez-Baltazar et al., 2017; Rossetti et al., 1988). The results show that DA neurons in nth-1;BY273 mutants were more resistant to 6-OHDA- and MPP+-induced neurotoxicity than DA neurons in BY273 animals (Figure 1E; Figure S1B).

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    Historically, mitochondrial dysfunction was linked to neurodegenerative conditions in the 1980s; patients who used drugs containing MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a known precursor to MPP+, which inhibits mitochondrial complex I in the electron transport chain (ETC), developed parkinsonism [3]. In this scenario, impaired mitochondria not only manifest diminished respiratory activity but also produce high ROS and RNS, resulting in oxidative and nitrosative stress [4,5]. Subsequent studies provided evidence that mitochondrial dysfunction is associated with mitochondrial DNA defects, disturbances in Ca2+ homeostasis, and abnormal mitochondrial morphology, thus playing a critical role in a variety of neurodegenerative conditions [6,7].

  • Metabolism of 1-methyl-4-phenyl-1,2,3/6-tetrahydropyridine by mitochondrion-targeted cytochrome P450 2D6 implications in parkinson disease

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    Within the dopaminergic neurons, MPP+ sequesters inside the mitochondrial compartment because of the positive charge it carries (8) and preferentially binds to and inhibits complex I of the electron transport chain (9). Inhibition of complex I leading to lower ATP generation (10), increased production of reactive oxygen species (ROS) (11, 12), and eventual cell death are believed to be the steps leading to Parkinson disease (13). Although MAO-B from glial cells is believed to be the main enzyme involved in the bioactivation of MPTP, cytochrome P450 2D6 (CYP2D6) is localized in the dopaminergic neurons of the substantia nigra (14) and has been suggested to be an important player in determining MPTP toxicity.

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Visiting Associate Professor from the Institute of Pharmacology, University of Cagliari, 09100 Cagliari, Italy.

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