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Medchem & Toxicology 2018
Page 77
Journal of Organic & Inorganic Chemistry
ISSN: 2472-1123
A n n u a l C o n g r e s s o n
Medicinal Chemistry,
Pharmacology and toxicology
J u l y 3 0 - 3 1 , 2 0 1 8
Am s t e r d a m , N e t h e r l a n d s
M
anganese (Mn) is a trace metal required for normal physiological processes in humans. Mn levels are tightly regulated, as
high levels of Mn results in accumulation in the brain and cause a neurological disease known as manganism. Manganism
shares many similarities with Parkinson’s disease (PD), both at the physiological level and the cellular level. Exposure to high
Mn-containing environments increases the risk of developing manganism. Homozygous mutations in
SLC30A10
cause familial
Parkinsonism associated with manganese (Mn) retention. We recently identified SLC30A10 to be a cell surface-localized Mn
efflux transporter and demonstrated that Parkinsonism causing mutations block its intracellular trafficking and efflux function.
In C. elegans, SLC30A10 over-expression protected against Mn-induced lethality and dopaminergic neurotoxicity, consistent with
results in mammalian systems. SLC30A10 expression did not protect worms against ZnSO
4
toxicity, suggesting that SLC30A10
does not mediate Zn export in
C. elegans.
Michael.Aschner@einstein.yu.eduManganese-induced neurotoxicity: lessons
from worms to human neonates
Michael Aschner
Albert Einstein College of Medicine, New York, USA
J Org Inorg Chem 2018, Volume 4
DOI: 10.21767/2472-1123-C3-009