| Bioactivity | MPP+ iodide, a toxic metabolite of the neurotoxin MPTP, causes symptom of Parkinson's disease in animal models by selectively destroying dopaminergic neurons in substantia nigra. MPP+ iodide is taken up by the dopamine transporter into dopaminergic neurons where it exerts its neurotoxic action on mitochondria by affecting complex I of the respiratory chain. MPP+ iodide is also a high affinity substrate for the serotonin transporter (SERT)[1][2]. |
| Invitro | MPP+ (1-3 mM; 24 hours) remarkably decreases the viability of cells[1].MPP+ also inhibits the activity of nicotinamide adenosine dinucleotide (NADH)-linked respiration in mitochondrial preparations and impairs aerobic glycolysis, leading to the present belief that the inhibition of NADH-linked cell respiration may constitute the final molecular mechanism of MPP+ neurotoxicity[3]. Cell Viability Assay[1] Cell Line: |
| Name | MPP+ iodide |
| CAS | 36913-39-0 |
| Formula | C12H12IN |
| Molar Mass | 297.14 |
| Appearance | Solid |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | 4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture) |
| Reference | [1]. Zhao M, et al. Mitochondrial calcium dysfunction contributes to autophagic cell death induced by MPP+ via AMPK pathway. Biochem Biophys Res Commun. 2019;509(2):390-394. [2]. Martí Y, et al. Methyl-4-phenylpyridinium (MPP+) differentially affects monoamine release and re-uptake in murine embryonic stem cell-derived dopaminergic and serotonergic neurons. Mol Cell Neurosci. 2017;83:37-45. [3]. Charlton CG. 1-Methyl-4-phenylpyridinium (MPP+) but not 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) serves as methyl donor for dopamine: a possible mechanism of action. J Geriatr Psychiatry Neurol. 1992;5(2):114-118. |