Literature DB >> 19660549

Mice deficient in dihydrolipoyl succinyl transferase show increased vulnerability to mitochondrial toxins.

Lichuan Yang1, Qingli Shi, Daniel J Ho, Anatoly A Starkov, Elizabeth J Wille, Hui Xu, H L Chen, Steven Zhang, Cliona M Stack, Noel Y Calingasan, Gary E Gibson, M Flint Beal.   

Abstract

The activity of a key mitochondrial tricarboxylic acid cycle enzyme, alpha-ketoglutarate dehydrogenase complex (KGDHC), declines in many neurodegenerative diseases. KGDHC consists of three subunits. The dihydrolipoyl succinyl transferase (DLST) component is unique to KGDHC. DLST(+/-) mice showed reduced mRNA and protein levels and decreased brain mitochondrial KGDHC activity. Neurotoxic effects of mitochondrial toxins were exacerbated in DLST(+/-) mice. MPTP produced a significantly greater reduction of striatal dopamine and tyrosine hydroxylase-positive neurons in the substantia nigra pars compacta of DLST(+/-) mice. DLST deficiency enhanced the severity of lipid peroxidation in the substantia nigra after MPTP treatment. Striatal lesions induced by either malonate or 3-nitropropionic acid (3-NP) were significantly larger in DLST(+/-) mice than in wildtype controls. DLST deficiency enhanced the 3-NP inhibition of mitochondria enzymes, and 3-NP induced protein and DNA oxidations. These observations support the hypothesis that reductions in KGDHC may impair the adaptability of the brain and contribute to the pathogenesis of neurodegenerative diseases.

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Year:  2009        PMID： 19660549      PMCID： PMC3605719          DOI： 10.1016/j.nbd.2009.07.023

Source DB:  PubMed          Journal:  Neurobiol Dis        ISSN： 0969-9961            Impact factor:   5.996


  53 in total

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2.  Lack of replication of association findings in complex disease: an analysis of 15 polymorphisms in prior candidate genes for sporadic Alzheimer's disease.

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Authors:  L C Park; D S Albers; H Xu; J G Lindsay; M F Beal; G E Gibson
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5.  Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions.

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Authors:  Peter Klivenyi; Anatoly A Starkov; Noel Y Calingasan; Gabrielle Gardian; Susan E Browne; Lichuan Yang; Parvesh Bubber; Gary E Gibson; Mulchand S Patel; M Flint Beal
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Authors:  Abraham M Brown; Derek Gordon; Hsinhwa Lee; Michael Caudy; Vahram Haroutunian; John P Blass
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  15 in total

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Journal:  Neurobiol Aging       Date:  2011-12-14       Impact factor: 4.673

2.  Brain [U-13 C]glucose metabolism in mice with decreased α-ketoglutarate dehydrogenase complex activity.

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3.  Recurrent Germline DLST Mutations in Individuals with Multiple Pheochromocytomas and Paragangliomas.

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Journal:  Mol Cell Neurosci       Date:  2012-07-20       Impact factor: 4.314

5.  Mild mitochondrial metabolic deficits by α-ketoglutarate dehydrogenase inhibition cause prominent changes in intracellular autophagic signaling: Potential role in the pathobiology of Alzheimer's disease.

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7.  Reductions in the mitochondrial enzyme α-ketoglutarate dehydrogenase complex in neurodegenerative disease - beneficial or detrimental?

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8.  The negative impact of α-ketoglutarate dehydrogenase complex deficiency on matrix substrate-level phosphorylation.

Authors:  Gergely Kiss; Csaba Konrad; Judit Doczi; Anatoly A Starkov; Hibiki Kawamata; Giovanni Manfredi; Steven F Zhang; Gary E Gibson; M Flint Beal; Vera Adam-Vizi; Christos Chinopoulos
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9.  The RNA-binding protein HuR is essential for the B cell antibody response.

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10.  Xanthoceraside ameliorates mitochondrial dysfunction contributing to the improvement of learning and memory impairment in mice with intracerebroventricular injection of aβ1-42.

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