Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1535, Issue 2, Pages 145-152Publisher
ELSEVIER
DOI: 10.1016/S0925-4439(00)00093-4
Keywords
acrolein; lipid peroxidation; mitochondria; neurodegeneration; Alzheimer's disease; respiration
Funding
- NIA NIH HHS [AG00774, AG16835] Funding Source: Medline
- NIEHS NIH HHS [ES05826] Funding Source: Medline
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Lipid peroxidation is elevated in diseased regions of brain in several neurodegenerative diseases. Acrolein (2-propenal) is a major cytotoxic product of lipid peroxidation and its adduction to neuronal proteins has been demonstrated in diseased brain regions from patients with Alzheimer's disease. Mitochondrial abnormalities are implicated in several neurodegenerative disorders, and mitochondria are targets of alkenal adduction in vivo. We examined the effects of acrolein upon multiple endpoints associated with the mitochondrial involvement in neurodegenerative disease. Acrolein inhibited state 3 respiration with an IC50 of approx. 0.4 mu mol/mg protein; however, there was no reduction in activity of complexes I-V. This inhibition was prevented by glutathione and N-acetylcysteine. Acrolein did not alter mitochondrial calcium transporter activity or induce cytochrome c release. These studies indicate that acrolein is a potent inhibitor of brain mitochondrial respiration. (C) 2001 Elsevier Science B.V. All rights reserved.
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