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Retention of the cyanobacterial neurotoxin β ‐ N ‐methylamino‐ l ‐alanine in melanin and neuromelanin‐containing cells – a possible link between Parkinson‐dementia complex and pigmentary retinopathy
Author(s) -
Karlsson Oskar,
Berg Cecilia,
Brittebo Eva B.,
Lindquist Nils Gunnar
Publication year - 2009
Publication title -
pigment cell and melanoma research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.618
H-Index - 105
eISSN - 1755-148X
pISSN - 1755-1471
DOI - 10.1111/j.1755-148x.2008.00508.x
Subject(s) - neuromelanin , melanin , neurotoxin , substantia nigra , biology , biochemistry , chemistry , microbiology and biotechnology , neuroscience , dopaminergic , dopamine
Summary β‐ N ‐methylamino‐ l ‐alanine (BMAA), a neurotoxic amino acid produced by cyanobacteria, has been suggested to be involved in the etiology of a neurodegenerative disease complex which includes Parkinson‐dementia complex (PDC). In PDC, neuromelanin‐containing neurons in substantia nigra are degenerated. Many PDC patients also have an uncommon pigmentary retinopathy. The aim of this study was to investigate the distribution of 3 H‐BMAA in mice and frogs, with emphasis on pigment‐containing tissues. Using autoradiography, a distinct retention of 3 H‐BMAA was observed in melanin‐containing tissues such as the eye and neuromelanin‐containing neurons in frog brain. Analysis of the binding of 3 H‐BMAA to Sepia melanin in vitro demonstrated two apparent binding sites. In vitro‐studies with synthetic melanin revealed a stronger interaction of 3 H‐BMAA with melanin during synthesis than the binding to preformed melanin. Long‐term exposure to BMAA may lead to bioaccumulation in melanin‐ and neuromelanin‐containing cells causing high intracellular levels, and potentially changed melanin characteristics via incorporation of BMAA into the melanin polymer. Interaction of BMAA with melanin may be a possible link between PDC and pigmentary retinopathy.