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Redox regulation of cellular stress response in aging and neurodegenerative disorders: role of vitagenes.
Neurochem Res 2007 Apr-May; 32(4-5):757-73NR

Abstract

Reduced expression and/or activity of antioxidant proteins lead to oxidative stress, accelerated aging and neurodegeneration. However, while excess reactive oxygen species (ROS) are toxic, regulated ROS play an important role in cell signaling. Perturbation of redox status, mutations favoring protein misfolding, altered glyc(osyl)ation, overloading of the product of polyunsaturated fatty acid peroxidation (hydroxynonenals, HNE) or cholesterol oxidation, can disrupt redox homeostasis. Collectively or individually these effects may impose stress and lead to accumulation of unfolded or misfolded proteins in brain cells. Alzheimer's (AD), Parkinson's and Huntington's disease, amyotrophic lateral sclerosis and Friedreich's ataxia are major neurological disorders associated with production of abnormally aggregated proteins and, as such, belong to the so-called "protein conformational diseases". The pathogenic aggregation of proteins in non-native conformation is generally associated with metabolic derangements and excessive production of ROS. The "unfolded protein response" has evolved to prevent accumulation of unfolded or misfolded proteins. Recent discoveries of the mechanisms of cellular stress signaling have led to new insights into the diverse processes that are regulated by cellular stress responses. The brain detects and overcomes oxidative stress by a complex network of "longevity assurance processes" integrated to the expression of genes termed vitagenes. Heat-shock proteins are highly conserved and facilitate correct protein folding. Heme oxygenase-1, an inducible and redox-regulated enzyme, has having an important role in cellular antioxidant defense. An emerging concept is neuroprotection afforded by heme oxygenase by its heme degrading activity and tissue-specific antioxidant effects, due to its products carbon monoxide and biliverdin, which is then reduced by biliverdin reductase in bilirubin. There is increasing interest in dietary compounds that can inhibit, retard or reverse the steps leading to neurodegeneration in AD. Specifically any dietary components that inhibit inappropriate inflammation, AbetaP oligomerization and consequent increased apoptosis are of particular interest, with respect to a chronic inflammatory response, brain injury and beta-amyloid associated pathology. Curcumin and ferulic acid, the first from the curry spice turmeric and the second a major constituent of fruit and vegetables, are candidates in this regard. Not only do these compounds serve as antioxidants but, in addition, they are strong inducers of the heat-shock response. Food supplementation with curcumin and ferulic acid are therefore being considered as a novel nutritional approach to reduce oxidative damage and amyloid pathology in AD. We review here some of the emerging concepts of pathways to neurodegeneration and how these may be overcome by a nutritional approach.

Authors+Show Affiliations

Section of Biochemistry and Molecular Biology, Department of Chemistry, Faculty of Medicine, University of Catania, Viale Andrea Doria 6, 95100, Catania, Italy. calabres@mbox.unict.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

17191135

Citation

Calabrese, Vittorio, et al. "Redox Regulation of Cellular Stress Response in Aging and Neurodegenerative Disorders: Role of Vitagenes." Neurochemical Research, vol. 32, no. 4-5, 2007, pp. 757-73.
Calabrese V, Guagliano E, Sapienza M, et al. Redox regulation of cellular stress response in aging and neurodegenerative disorders: role of vitagenes. Neurochem Res. 2007;32(4-5):757-73.
Calabrese, V., Guagliano, E., Sapienza, M., Panebianco, M., Calafato, S., Puleo, E., ... Stella, A. G. (2007). Redox regulation of cellular stress response in aging and neurodegenerative disorders: role of vitagenes. Neurochemical Research, 32(4-5), pp. 757-73.
Calabrese V, et al. Redox Regulation of Cellular Stress Response in Aging and Neurodegenerative Disorders: Role of Vitagenes. Neurochem Res. 2007;32(4-5):757-73. PubMed PMID: 17191135.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Redox regulation of cellular stress response in aging and neurodegenerative disorders: role of vitagenes. AU - Calabrese,Vittorio, AU - Guagliano,Eleonora, AU - Sapienza,Maria, AU - Panebianco,Mariangela, AU - Calafato,Stella, AU - Puleo,Edoardo, AU - Pennisi,Giovanni, AU - Mancuso,Cesare, AU - Butterfield,D Allan, AU - Stella,Annamaria Giuffrida, Y1 - 2006/12/27/ PY - 2006/09/26/received PY - 2006/10/11/accepted PY - 2006/12/28/pubmed PY - 2007/5/30/medline PY - 2006/12/28/entrez SP - 757 EP - 73 JF - Neurochemical research JO - Neurochem. Res. VL - 32 IS - 4-5 N2 - Reduced expression and/or activity of antioxidant proteins lead to oxidative stress, accelerated aging and neurodegeneration. However, while excess reactive oxygen species (ROS) are toxic, regulated ROS play an important role in cell signaling. Perturbation of redox status, mutations favoring protein misfolding, altered glyc(osyl)ation, overloading of the product of polyunsaturated fatty acid peroxidation (hydroxynonenals, HNE) or cholesterol oxidation, can disrupt redox homeostasis. Collectively or individually these effects may impose stress and lead to accumulation of unfolded or misfolded proteins in brain cells. Alzheimer's (AD), Parkinson's and Huntington's disease, amyotrophic lateral sclerosis and Friedreich's ataxia are major neurological disorders associated with production of abnormally aggregated proteins and, as such, belong to the so-called "protein conformational diseases". The pathogenic aggregation of proteins in non-native conformation is generally associated with metabolic derangements and excessive production of ROS. The "unfolded protein response" has evolved to prevent accumulation of unfolded or misfolded proteins. Recent discoveries of the mechanisms of cellular stress signaling have led to new insights into the diverse processes that are regulated by cellular stress responses. The brain detects and overcomes oxidative stress by a complex network of "longevity assurance processes" integrated to the expression of genes termed vitagenes. Heat-shock proteins are highly conserved and facilitate correct protein folding. Heme oxygenase-1, an inducible and redox-regulated enzyme, has having an important role in cellular antioxidant defense. An emerging concept is neuroprotection afforded by heme oxygenase by its heme degrading activity and tissue-specific antioxidant effects, due to its products carbon monoxide and biliverdin, which is then reduced by biliverdin reductase in bilirubin. There is increasing interest in dietary compounds that can inhibit, retard or reverse the steps leading to neurodegeneration in AD. Specifically any dietary components that inhibit inappropriate inflammation, AbetaP oligomerization and consequent increased apoptosis are of particular interest, with respect to a chronic inflammatory response, brain injury and beta-amyloid associated pathology. Curcumin and ferulic acid, the first from the curry spice turmeric and the second a major constituent of fruit and vegetables, are candidates in this regard. Not only do these compounds serve as antioxidants but, in addition, they are strong inducers of the heat-shock response. Food supplementation with curcumin and ferulic acid are therefore being considered as a novel nutritional approach to reduce oxidative damage and amyloid pathology in AD. We review here some of the emerging concepts of pathways to neurodegeneration and how these may be overcome by a nutritional approach. SN - 0364-3190 UR - https://www.unboundmedicine.com/medline/citation/17191135/Redox_regulation_of_cellular_stress_response_in_aging_and_neurodegenerative_disorders:_role_of_vitagenes_ L2 - https://doi.org/10.1007/s11064-006-9203-y DB - PRIME DP - Unbound Medicine ER -