Open AccessCoenzyme Q 10 inhibits mitochondrial complex‐1 down‐regulation and nuclear factor‐kappa B activation
Author(s) -
Ebadi M.,
Sharma S. K.,
Wanpen S.,
Amornpan A.
Publication year - 2004
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2004.tb00276.x
Subject(s) - rotenone , neuroprotection , neurodegeneration , biology , striatum , coenzyme q – cytochrome c reductase , dopamine , mitochondrion , chemistry , endocrinology , biochemistry , medicine , neuroscience , cytochrome c , disease
We have used control‐homozygous weaver mutant, and ‐heterozygous weaver mutant mice in order to explore the basic molecular mechanism of neurodegeneration and the neuroprotective potential of coenzyme Q 10 . Homozygous weaver mutant mice exhibited progressive neurodegeneration in the hippocampus, striatum, and cerebellum, and a reduction in the striatal levels of dopamine and coenzyme Qs (Q 9 and Q 10 ) without any significant changes in norepinephrine and serotonin. Mitochondrial complex‐1 was down regulated; whereas nuclear factor‐kappa B was up regulated in homozygous weaver mutant mice. Rotenone inhibited complex‐1, enhanced nuclear factor‐kappa B, and caused apoptosis in human dopaminergic (SK‐N‐SH) neurons; whereas nuclear factor‐kappa B antibody suppressed rotenone‐induced apoptosis, suggesting that enhancing coenzyme Q 10 synthesis and suppressing the induction of NF‐kappa B, may provide neuroprotection.