TY - JOUR
T1 - Ectopic deposition of melanin pigments as detoxifying mechanism
T2 - A paradigm for basal nuclei pigmentation
AU - De Marco, Federico
AU - Foppoli, Cesira
AU - Coccia, Raffaella
AU - Blarzino, Carla
AU - Perluigi, Marzia
AU - Cini, Chiara
AU - Marcante, Maria Luisa
PY - 2004/2/6
Y1 - 2004/2/6
N2 - Melanins are UV shielding pigments found in skin and other light exposed tissues. However, a kind of melanin, named neuromelanin (NM), is found in those deep brain loci that degenerate in Parkinson's disease (PD), where no such a function may be imagined. The NM synthetic pathway, different from the one of eumelanin based on tyrosinase, is still obscure as well as its physiological function. Here we show that under conditions of excess of toxic quinone concentration, nonmelanocytic cell strains (i.e., primary keratinocytes) may accumulate a dark cytoplasmatic pigment that proved to be a melanin. The ability of pigment deposition, possibly driven by peroxidases, is restricted to diploid cells and increases cell survival acting as a sink for potentially hazardous quinones. We suggest that in the basal nuclei, exposed to high level of catecholaminergic neurotransmitters, NM deposition is a relevant antioxidant mechanism by trapping quinones and semiquinones, thus protecting neurons from accumulating damage over many years. In this perspective, just as a hypothesis, we may imagine that PD neuron degeneration is the consequence of a reduced/abrogated ability to produce neuromelanin.
AB - Melanins are UV shielding pigments found in skin and other light exposed tissues. However, a kind of melanin, named neuromelanin (NM), is found in those deep brain loci that degenerate in Parkinson's disease (PD), where no such a function may be imagined. The NM synthetic pathway, different from the one of eumelanin based on tyrosinase, is still obscure as well as its physiological function. Here we show that under conditions of excess of toxic quinone concentration, nonmelanocytic cell strains (i.e., primary keratinocytes) may accumulate a dark cytoplasmatic pigment that proved to be a melanin. The ability of pigment deposition, possibly driven by peroxidases, is restricted to diploid cells and increases cell survival acting as a sink for potentially hazardous quinones. We suggest that in the basal nuclei, exposed to high level of catecholaminergic neurotransmitters, NM deposition is a relevant antioxidant mechanism by trapping quinones and semiquinones, thus protecting neurons from accumulating damage over many years. In this perspective, just as a hypothesis, we may imagine that PD neuron degeneration is the consequence of a reduced/abrogated ability to produce neuromelanin.
KW - Human keratinocytes
KW - Melanin
KW - Neuromelanin
KW - Parkinson's disease
KW - Peroxidase
KW - Tetrahydropapaveroline
UR - http://www.scopus.com/inward/record.url?scp=0345743588&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0345743588&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2003.12.127
DO - 10.1016/j.bbrc.2003.12.127
M3 - Article
C2 - 14733954
AN - SCOPUS:0345743588
VL - 314
SP - 631
EP - 637
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -