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Mitochondrial decay in the aging rat heart: evidence for improvement by dietary supplementation with acetyl-L-carnitine and/or lipoic acid.
Ann N Y Acad Sci. 2002 Apr; 959:491-507.AN

Abstract

Mitochondrial decay has been postulated to be a significant underlying part of the aging process. Decline in mitochondrial function may lead to cellular energy deficits, especially in times of greater energy demand, and compromise vital ATP-dependent cellular operations, including detoxification, repair systems, DNA replication, and osmotic balance. Mitochondrial decay may also lead to enhanced oxidant production and thus render the cell more prone to oxidative insult. In particular, the heart may be especially susceptible to mitochondrial dysfunction due to myocardial dependency on beta-oxidation of fatty acids for energy and the postmitotic nature of cardiac myocytes, which would allow for greater accumulation of mitochondrial mutations and deletions. Thus, maintenance of mitochondrial function may be important to maintain overall myocardial function. Herein, we review the major age-related changes that occur to mitochondria in the aging heart and the evidence that two such supplements, acetyl-l-carnitine (ALCAR) and (R)-alpha-lipoic acid, may improve myocardial bioenergetics and lower the increased oxidative stress associated with aging. We and others have shown that feeding old rats ALCAR reverses the age-related decline in carnitine levels and improves mitochondrial beta-oxidation in a number of tissues studied. However, ALCAR supplementation does not appear to reverse the age-related decline in cardiac antioxidant status and thus may not substantially alter indices of oxidative stress. Lipoic acid, a potent thiol antioxidant and mitochondrial metabolite, appears to increase low molecular weight antioxidant status and thereby decreases age-associated oxidative insult. Thus, ALCAR along with lipoic acid may be effective supplemental regimens to maintain myocardial function.

Authors+Show Affiliations

Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, Oregon 97331, USA. tory.hagen@orst.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

11976222

Citation

Hagen, Tory M., et al. "Mitochondrial Decay in the Aging Rat Heart: Evidence for Improvement By Dietary Supplementation With acetyl-L-carnitine And/or Lipoic Acid." Annals of the New York Academy of Sciences, vol. 959, 2002, pp. 491-507.
Hagen TM, Moreau R, Suh JH, et al. Mitochondrial decay in the aging rat heart: evidence for improvement by dietary supplementation with acetyl-L-carnitine and/or lipoic acid. Ann N Y Acad Sci. 2002;959:491-507.
Hagen, T. M., Moreau, R., Suh, J. H., & Visioli, F. (2002). Mitochondrial decay in the aging rat heart: evidence for improvement by dietary supplementation with acetyl-L-carnitine and/or lipoic acid. Annals of the New York Academy of Sciences, 959, 491-507.
Hagen TM, et al. Mitochondrial Decay in the Aging Rat Heart: Evidence for Improvement By Dietary Supplementation With acetyl-L-carnitine And/or Lipoic Acid. Ann N Y Acad Sci. 2002;959:491-507. PubMed PMID: 11976222.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondrial decay in the aging rat heart: evidence for improvement by dietary supplementation with acetyl-L-carnitine and/or lipoic acid. AU - Hagen,Tory M, AU - Moreau,Régis, AU - Suh,Jung H, AU - Visioli,Francesco, PY - 2002/4/27/pubmed PY - 2002/6/5/medline PY - 2002/4/27/entrez SP - 491 EP - 507 JF - Annals of the New York Academy of Sciences JO - Ann N Y Acad Sci VL - 959 N2 - Mitochondrial decay has been postulated to be a significant underlying part of the aging process. Decline in mitochondrial function may lead to cellular energy deficits, especially in times of greater energy demand, and compromise vital ATP-dependent cellular operations, including detoxification, repair systems, DNA replication, and osmotic balance. Mitochondrial decay may also lead to enhanced oxidant production and thus render the cell more prone to oxidative insult. In particular, the heart may be especially susceptible to mitochondrial dysfunction due to myocardial dependency on beta-oxidation of fatty acids for energy and the postmitotic nature of cardiac myocytes, which would allow for greater accumulation of mitochondrial mutations and deletions. Thus, maintenance of mitochondrial function may be important to maintain overall myocardial function. Herein, we review the major age-related changes that occur to mitochondria in the aging heart and the evidence that two such supplements, acetyl-l-carnitine (ALCAR) and (R)-alpha-lipoic acid, may improve myocardial bioenergetics and lower the increased oxidative stress associated with aging. We and others have shown that feeding old rats ALCAR reverses the age-related decline in carnitine levels and improves mitochondrial beta-oxidation in a number of tissues studied. However, ALCAR supplementation does not appear to reverse the age-related decline in cardiac antioxidant status and thus may not substantially alter indices of oxidative stress. Lipoic acid, a potent thiol antioxidant and mitochondrial metabolite, appears to increase low molecular weight antioxidant status and thereby decreases age-associated oxidative insult. Thus, ALCAR along with lipoic acid may be effective supplemental regimens to maintain myocardial function. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/11976222/Mitochondrial_decay_in_the_aging_rat_heart:_evidence_for_improvement_by_dietary_supplementation_with_acetyl_L_carnitine_and/or_lipoic_acid_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0077-8923&date=2002&volume=959&spage=491 DB - PRIME DP - Unbound Medicine ER -