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Neuroprotective role for carbonyl reductase?
Biochem Biophys Res Commun 2006; 340(4):1019-22BB

Abstract

Oxidative stress is increasingly implicated in neurodegenerative disorders including Alzheimer's, Parkinson's, Huntington's, and Creutzfeld-Jakob diseases or amyotrophic lateral sclerosis. Reactive oxygen species seem to play a significant role in neuronal cell death in that they generate reactive aldehydes from membrane lipid peroxidation. Several neuronal diseases are associated with increased accumulation of abnormal protein adducts of reactive aldehydes, which mediate oxidative stress-linked pathological events, including cellular growth inhibition and apoptosis induction. Combining findings on neurodegeneration and oxidative stress in Drosophila with studies on the metabolic characteristics of the human enzyme carbonyl reductase (CR), it is clear now that CR has a potential physiological role for neuroprotection in humans. Several lines of evidence suggest that CR represents a significant pathway for the detoxification of reactive aldehydes derived from lipid peroxidation and that CR in humans is essential for neuronal cell survival and to confer protection against oxidative stress-induced brain degeneration.

Authors+Show Affiliations

Institute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Brunswiker Str. 10, 24105 Kiel, Germany. maser@toxi.uni-kiel.de

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

16406002

Citation

Maser, Edmund. "Neuroprotective Role for Carbonyl Reductase?" Biochemical and Biophysical Research Communications, vol. 340, no. 4, 2006, pp. 1019-22.
Maser E. Neuroprotective role for carbonyl reductase? Biochem Biophys Res Commun. 2006;340(4):1019-22.
Maser, E. (2006). Neuroprotective role for carbonyl reductase? Biochemical and Biophysical Research Communications, 340(4), pp. 1019-22.
Maser E. Neuroprotective Role for Carbonyl Reductase. Biochem Biophys Res Commun. 2006 Feb 24;340(4):1019-22. PubMed PMID: 16406002.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective role for carbonyl reductase? A1 - Maser,Edmund, Y1 - 2005/12/28/ PY - 2005/12/08/received PY - 2005/12/20/accepted PY - 2006/1/13/pubmed PY - 2006/3/22/medline PY - 2006/1/13/entrez SP - 1019 EP - 22 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 340 IS - 4 N2 - Oxidative stress is increasingly implicated in neurodegenerative disorders including Alzheimer's, Parkinson's, Huntington's, and Creutzfeld-Jakob diseases or amyotrophic lateral sclerosis. Reactive oxygen species seem to play a significant role in neuronal cell death in that they generate reactive aldehydes from membrane lipid peroxidation. Several neuronal diseases are associated with increased accumulation of abnormal protein adducts of reactive aldehydes, which mediate oxidative stress-linked pathological events, including cellular growth inhibition and apoptosis induction. Combining findings on neurodegeneration and oxidative stress in Drosophila with studies on the metabolic characteristics of the human enzyme carbonyl reductase (CR), it is clear now that CR has a potential physiological role for neuroprotection in humans. Several lines of evidence suggest that CR represents a significant pathway for the detoxification of reactive aldehydes derived from lipid peroxidation and that CR in humans is essential for neuronal cell survival and to confer protection against oxidative stress-induced brain degeneration. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/16406002/Neuroprotective_role_for_carbonyl_reductase L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(05)02876-7 DB - PRIME DP - Unbound Medicine ER -