Abstract
Reactive oxygen species and reactive nitrogen species promote endothelial dysfunction in old ageand contribute to the development of cardiovascular diseases such as atherosclerosis, diabetes, and hypertension. α-lipoic acid was identified as a catalytic agent for oxidative decarboxylation of pyruvate and α-ketoglutarate in 1951, and it has been studied intensively by chemists, biologists, and clinicians who have been interested in its role in energetic metabolism and protection from reactive oxygen species-induced mitochondrial dysfunction. Consequently, many biological effects of α- lipoic acid supplementation can be attributed to the potent antioxidant properties of α-lipoic acid and dihydro α-lipoic acid. The reducing environments inside the cell help to protect from oxidative damage and the reduction-oxidation status of α-lipoic acid is dependent upon the degree to which the cellular components are found in the oxidized state. Although healthy young humans can synthesize enough α-lipoic acid to scavenge reactive oxygen species and enhance endogenous antioxidants like glutathione and vitamins C and E, the level of α-lipoic acid significantly declines with age and this may lead to endothelial dysfunction. Furthermore, many studies have reported α-lipoic acid can regulate the transcription of genes associated with anti-oxidant and anti-inflammatory pathways. In this review, we will discuss recent clinical studies that have investigated the beneficial effects of α-lipoic acid on endothelial dysfunction and propose possible mechanisms involved.
Keywords: α-keto acid dehydrogenase complex, Cardiovascular disease, Endothelial dysfunction, Glutathione, Glycine cleavage enzyme, Reactive oxygen species, Thiol-disulfide, Thioredoxin.
Current Medicinal Chemistry
Title:Physiological Effect and Therapeutic Application of Alpha Lipoic Acid
Volume: 21 Issue: 32
Author(s): Sungmi Park, Udayakumar Karunakaran, Nam Ho Jeoung, Jae-Han Jeon and In-Kyu Lee
Affiliation:
Keywords: α-keto acid dehydrogenase complex, Cardiovascular disease, Endothelial dysfunction, Glutathione, Glycine cleavage enzyme, Reactive oxygen species, Thiol-disulfide, Thioredoxin.
Abstract: Reactive oxygen species and reactive nitrogen species promote endothelial dysfunction in old ageand contribute to the development of cardiovascular diseases such as atherosclerosis, diabetes, and hypertension. α-lipoic acid was identified as a catalytic agent for oxidative decarboxylation of pyruvate and α-ketoglutarate in 1951, and it has been studied intensively by chemists, biologists, and clinicians who have been interested in its role in energetic metabolism and protection from reactive oxygen species-induced mitochondrial dysfunction. Consequently, many biological effects of α- lipoic acid supplementation can be attributed to the potent antioxidant properties of α-lipoic acid and dihydro α-lipoic acid. The reducing environments inside the cell help to protect from oxidative damage and the reduction-oxidation status of α-lipoic acid is dependent upon the degree to which the cellular components are found in the oxidized state. Although healthy young humans can synthesize enough α-lipoic acid to scavenge reactive oxygen species and enhance endogenous antioxidants like glutathione and vitamins C and E, the level of α-lipoic acid significantly declines with age and this may lead to endothelial dysfunction. Furthermore, many studies have reported α-lipoic acid can regulate the transcription of genes associated with anti-oxidant and anti-inflammatory pathways. In this review, we will discuss recent clinical studies that have investigated the beneficial effects of α-lipoic acid on endothelial dysfunction and propose possible mechanisms involved.
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Cite this article as:
Park Sungmi, Karunakaran Udayakumar, Jeoung Ho Nam, Jeon Jae-Han and Lee In-Kyu, Physiological Effect and Therapeutic Application of Alpha Lipoic Acid, Current Medicinal Chemistry 2014; 21 (32) . https://dx.doi.org/10.2174/0929867321666140706141806
DOI https://dx.doi.org/10.2174/0929867321666140706141806 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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