Mitochondrial 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 | Zendy

Christian T. Sheline | Zendy; Julia Zhu | Zendy; Wendy Zhang | Zendy; Chunxiao Shi | Zendy; Aili Cai | Zendy

Open Access

Mitochondrial 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.

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