Tags

Type your tag names separated by a space and hit enter

Redox modulation of heat shock protein expression by acetylcarnitine in aging brain: relationship to antioxidant status and mitochondrial function.
Antioxid Redox Signal. 2006 Mar-Apr; 8(3-4):404-16.AR

Abstract

There is significant evidence to show that aging is characterized by a stochastic accumulation of molecular damage and by a progressive failure of maintenance and repair processes. Protective mechanisms exist in the brain which are controlled by vitagenes and include members of the heat shock system, heme oxygenase-I, and Hsp70 as critical determinants of brain stress tolerance. Given the broad cytoprotective properties of the heat shock response, molecules inducing this defense mechanism appear to be possible candidates for novel cytoprotective strategies. Acetyl-L-carnitine is proposed as a therapeutic agent for several neurodegenerative disorders, and the present study reports that treatment for 4 months of senescent rats with acetyl-L-carnitine induces heme oxygenase-1 as well as Hsp70 and SOD-2. This effect was associated with upregulation of GSH levels, prevention of age-related changes in mitochondrial respiratory chain complex expression, and decrease in protein carbonyls and HNE formation. We hypothesize that maintenance or recovery of the activity of vitagenes may delay the aging process and decrease the risk of age-related diseases. Particularly, modulation of endogenous cellular defense mechanisms via acetyl-L-carnitine may represent an innovative approach to therapeutic intervention in diseases causing tissue damage, such as neurodegeneration.

Authors+Show Affiliations

Section of Biochemistry and Molecular Biology, Department of Chemistry, Faculty of Medicine, University of Catania, Catania, Italy.No 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

Language

eng

PubMed ID

16677087

Citation

Calabrese, V, et al. "Redox Modulation of Heat Shock Protein Expression By Acetylcarnitine in Aging Brain: Relationship to Antioxidant Status and Mitochondrial Function." Antioxidants & Redox Signaling, vol. 8, no. 3-4, 2006, pp. 404-16.
Calabrese V, Colombrita C, Sultana R, et al. Redox modulation of heat shock protein expression by acetylcarnitine in aging brain: relationship to antioxidant status and mitochondrial function. Antioxid Redox Signal. 2006;8(3-4):404-16.
Calabrese, V., Colombrita, C., Sultana, R., Scapagnini, G., Calvani, M., Butterfield, D. A., & Stella, A. M. (2006). Redox modulation of heat shock protein expression by acetylcarnitine in aging brain: relationship to antioxidant status and mitochondrial function. Antioxidants & Redox Signaling, 8(3-4), 404-16.
Calabrese V, et al. Redox Modulation of Heat Shock Protein Expression By Acetylcarnitine in Aging Brain: Relationship to Antioxidant Status and Mitochondrial Function. Antioxid Redox Signal. 2006 Mar-Apr;8(3-4):404-16. PubMed PMID: 16677087.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Redox modulation of heat shock protein expression by acetylcarnitine in aging brain: relationship to antioxidant status and mitochondrial function. AU - Calabrese,V, AU - Colombrita,C, AU - Sultana,R, AU - Scapagnini,G, AU - Calvani,M, AU - Butterfield,D A, AU - Stella,A M Giuffrida, PY - 2006/5/9/pubmed PY - 2006/9/9/medline PY - 2006/5/9/entrez SP - 404 EP - 16 JF - Antioxidants & redox signaling JO - Antioxid. Redox Signal. VL - 8 IS - 3-4 N2 - There is significant evidence to show that aging is characterized by a stochastic accumulation of molecular damage and by a progressive failure of maintenance and repair processes. Protective mechanisms exist in the brain which are controlled by vitagenes and include members of the heat shock system, heme oxygenase-I, and Hsp70 as critical determinants of brain stress tolerance. Given the broad cytoprotective properties of the heat shock response, molecules inducing this defense mechanism appear to be possible candidates for novel cytoprotective strategies. Acetyl-L-carnitine is proposed as a therapeutic agent for several neurodegenerative disorders, and the present study reports that treatment for 4 months of senescent rats with acetyl-L-carnitine induces heme oxygenase-1 as well as Hsp70 and SOD-2. This effect was associated with upregulation of GSH levels, prevention of age-related changes in mitochondrial respiratory chain complex expression, and decrease in protein carbonyls and HNE formation. We hypothesize that maintenance or recovery of the activity of vitagenes may delay the aging process and decrease the risk of age-related diseases. Particularly, modulation of endogenous cellular defense mechanisms via acetyl-L-carnitine may represent an innovative approach to therapeutic intervention in diseases causing tissue damage, such as neurodegeneration. SN - 1523-0864 UR - https://www.unboundmedicine.com/medline/citation/16677087/Redox_modulation_of_heat_shock_protein_expression_by_acetylcarnitine_in_aging_brain:_relationship_to_antioxidant_status_and_mitochondrial_function_ L2 - https://www.liebertpub.com/doi/full/10.1089/ars.2006.8.404?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -