Open AccessMitochondrial Inhibitor Models of Huntington’s Disease and Parkinson’s Disease Induce Zinc Accumulation and Are Attenuated by Inhibition of Zinc Neurotoxicity in vitro or in vivo
Author(s) -
Christian T. Sheline,
Julia Zhu,
Wendy Zhang,
Chunxiao Shi,
Aili Cai
Publication year - 2012
Publication title -
neurodegenerative diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.98
H-Index - 57
eISSN - 1660-2862
pISSN - 1660-2854
DOI - 10.1159/000336558
Subject(s) - nad+ kinase , nicotinamide adenine dinucleotide , neurotoxicity , neuroprotection , nicotinamide , biochemistry , glycolysis , tyrosine hydroxylase , in vivo , chemistry , mitochondrion , pharmacology , neurodegeneration , striatum , biology , dopamine , metabolism , endocrinology , medicine , enzyme , toxicity , microbiology and biotechnology , organic chemistry , disease
Inhibition of mitochondrial function occurs in many neurodegenerative diseases, and inhibitors of mitochondrial complexes I and II are used to model them. The complex II inhibitor, 3-nitroproprionic acid (3-NPA), kills the striatal neurons susceptible in Huntington's disease. The complex I inhibitor N-methyl-4-phenylpyridium (MPP(+)) and 6-hydroxydopamine (6-OHDA) are used to model Parkinson's disease. Zinc (Zn(2+)) accumulates after 3-NPA, 6-OHDA and MPP(+) in situ or in vivo.