Inflaming the diseased brain: a role for tainted melanins.

TitleInflaming the diseased brain: a role for tainted melanins.
Publication TypeJournal Article
Year of Publication2015
AuthorsJeitner TM, Kalogiannis M, Patrick PA, Gomolin I, Palaia T, Ragolia L, Brand D, Delikatny EJ
JournalBiochim Biophys Acta
Volume1852
Issue5
Pagination937-50
Date Published2015 May
ISSN0006-3002
KeywordsAnimals, Apoptosis, Brain, Brain Chemistry, Cell Line, Tumor, Dopamine, Halogenation, Humans, Hypochlorous Acid, Immunohistochemistry, Inflammation, Male, Melanins, Mice, Inbred C57BL, Microscopy, Electron, Phagocytes, Phagocytosis, Spectrophotometry, Tumor Necrosis Factor-alpha, Tyrosine 3-Monooxygenase
Abstract

Inflammation plays a crucial role in neurodegenerative diseases, but the irritants responsible for this response remain largely unknown. This report addressed the hypothesis that hypochlorous acid reacts with dopamine to produce melanic precipitates that promote cerebral inflammation. Spectrophotometric studies demonstrated that nM amounts of HOCl and dopamine react within seconds. A second-order rate constant for the reaction of HOCl and dopamine of 2.5 × 10(4)M(-1)s(-1) was obtained by measuring loss of dopaminergic fluorescence due to HOCl. Gravimetric measurements, electron microscopy, elemental analysis, and a novel use of flow cytometry confirmed that the major product of this reaction is a precipitate with an average diameter of 1.5 μm. Flow cytometry was also used to demonstrate the preferential reaction of HOCl with dopamine rather than albumin. Engulfment of the chlorodopamine particulates by phagocytes in vitro caused these cells to release TNFα and die. Intrastriatal administration of 10(6) particles also increased the content of TNFα in the brain and led to a 50% loss of the dopaminergic neurons in the nigra. These studies indicate that HOCl and dopamine react quickly and preferentially with each other to produce particles that promote inflammation and neuronal death in the brain.

DOI10.1016/j.bbadis.2015.01.004
Alternate JournalBiochim Biophys Acta
PubMed ID25585261
PubMed Central IDPMC5113040
Grant ListR03 NS074286 / NS / NINDS NIH HHS / United States
R03-N3074286 / / PHS HHS / United States
Related Institute: 
Molecular Imaging Innovations Institute (MI3)

Weill Cornell Medicine
Department of Radiology
525 East 68th Street New York, NY 10065