1: Arzneimittelforschung. 1998 Jan;48(1):13-21. Related Articles, Links
Cardioprotective effects of dihydrolipoic acid and tocopherol in right heart hypertrophy during oxidative stress.
Thurich T, Bereiter-Hahn J, Schneider M, Zimmer G.
Gustav-Embden-Zentrum der Biologischen Chemie, Arbeitsgruppe Membranstruktur.
Rat hearts hypertrophied by exposure of the animals to low oxygen pressure were perfused by the Langendorff technique. After oxidative stress induced by hypoxia/reoxygenation, functional recovery of the hypertrophied right heart was insufficient when compared to non-hypertrophied controls. Accordingly, mitochondrial membrane potential did not recover sufficiently. There was a positive trend for improvement of the rate-pressure product during reoxygenation in lipoic acid (CAS 1077-28-7; 0.8 mumol/l) treated hearts which was also verified for membrane potential. Adenosine 5'-triphosphate and creatine phosphate contents as well as the ATP/ADP ratio in hypertrophied right ventricle were significantly increased after reoxygenation in hearts treated with lipoic acid.
With lipoic acid, there was a significantly higher content of glutathione (oxidized form) after reoxygenation, Ca2+ uptake was significantly increased in mitochondria isolated from hypertrophied right ventricles and treated by 12 nmol/mg protein of lipoic acid. The results reveal a distinct improvement of mitochondrial structure/function by lipoic acid and suggest for therapy a combination with the synergistic free radical scavenging properties of tocopherol (CAS 10191-41-0).
PMID: 9522025 [PubMed - indexed for MEDLINE]
Regarding Acetyl-Lcarnitine:
1: Ann N Y Acad Sci. 2002 Apr;959:491-507. Related Articles, Links
Mitochondrial decay in the aging rat heart: evidence for improvement by dietary supplementation with acetyl-L-carnitine and/or lipoic acid.
Hagen TM, Moreau R, Suh JH, Visioli F.
Department of Biochemistry and Biophysics, Linus Pauling Institute, Oregon State University, Corvallis, Oregon 97331, USA.
[email protected]
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.Publication Types:
Review
Review, Tutorial
PMID: 11976222 [PubMed - indexed for MEDLINE]
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