Anticholesterol Activity of α-Lipoic Acid

Angelucci, L.; Mascitelli-Coriandoli, E

doi:10.1038/181911b0

Cited by 18 publications

(3 citation statements)

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“…However, the effect of exogenous LA on plasma cholesterol levels in animal models has produced conflicting data [4, 5, 8–10]. Plasma cholesterol levels are significantly higher in Lias +/− ApoE −/− mice than Lias +/+ ApoE −/− mice, although linear regression analysis indicates that a high plasma cholesterol level is not a major contributing factor to atherosclerosis development in our animals.…”

Section: Discussionmentioning

confidence: 91%

“…However, results in the literature are somewhat conflicting with some studies suggesting that LA also exhibits pro-oxidant properties [7]. Controversy also persists with regards to plasma cholesterol, with one set of work suggesting LA acts to reduce the sterol [5, 8, 9], while another set reports the absence of any such effect [4, 10]. Such discrepancies may stem from differing routes of LA administration as well as other pharmacokinetic and pharmaceutical factors.…”

Section: Introductionmentioning

confidence: 99%

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Genetic reduction of lipoic acid synthase expression modestly increases atherosclerosis in male, but not in female, apolipoprotein E-deficient mice

Kim

et al. 2010

Atherosclerosis

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Objectives-To evaluate the effects of a genetic reduction of Lias gene expression on atherosclerosis development.Methods and Results-Heterozygous knockout mice for the lipoid acid synthase gene (Lias +/− ) were crossed with apolipoprotein E-deficient (ApoE −/− ) mice, and the plaque size in aortic sinuses of Lias +/− ApoE −/− mice was evaluated at 6 months of age. Lesions at the aortic sinus in Lias +/− ApoE −/− males were significantly larger (1.5X) than those in Lias +/+ ApoE −/− littermate males. The lesion size was inversely correlated with an increased erythrocyte reduced glutathione/ oxidized glutathione (GSH/GSSH) ratio, an systemic index of body redox balance. Lias +/− ApoE −/− males also had significantly increased plasma cholesterol and reduced pyruvate dehydrogenase complex activity in the liver. Significant reductions in the expression of genes for antioxidant enzymes, including superoxide dismutase 1 (SOD1) and SOD2, were observed in aortas of Lias +/− ApoE −/− males. Female Lias +/− ApoE −/− also exhibited changes in these parameters, parallel to those observed in males. However, the Lias gene effects for the majority of these factors, including atherosclerotic lesion size, were not significant in females.Conclusions-Our data provide evidence that Lias deficiency enhances atherosclerosis in male mice, at least in part due to reduce antioxidant capacity. The notable absence of such effects in females leaves open the possibility of a gender-specific protection mechanism.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Genetic reduction of lipoic acid synthase expression modestly increases atherosclerosis in male, but not in female, apolipoprotein E-deficient mice

Kim

et al. 2010

Atherosclerosis

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“…One mechanism underlying increased risk for AD due to the presence of apoE4 is that apoE4 is less effective in transporting cholesterol than apoE3 when neurons respond to neuronal stress, including beta-amyloid toxicity, oxygen deficiency, oxidative damage, and head trauma, all of which require neuronal repair (Raffai and Weisgraber 2003). LA has anti-cholesterol activity (Angelucci and Mascitelli-Coriandoli 1958, Kritchevsky and Moyer 1958, Jayanthi and Varalakshmi 1992. ALCAR reduces age-associated increases in cholesterol in rat brain and blood (Ruggiero et al 1990, Aureli et al 2000.…”

Section: Effectiveness Of Combinations Of Mt-nutrient Supplementationmentioning

confidence: 99%

Reducing mitochondrial decay with mitochondrial nutrients to delay and treat cognitive dysfunction, Alzheimer's disease, and Parkinson's disease

Liu¹,

Ames²

2005

Nutritional Neuroscience

127

116

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Mitochondrial decay due to oxidative damage is a contributor to brain aging and age-related neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD). One type of mitochondrial decay is oxidative modification of key mitochondrial enzymes. Enzyme dysfunction, that is due to poor binding of substrates and coenzymes may be ameliorated by supplementing adequate levels of substrates or coenzyme precursors. Such supplementation with mitochondrial nutrients (mt-nutrients) may be useful to prevent or delay mitochondrial decay, thus prevent or treat AD and PD. In the present review, we survey the literature to identify mt-nutrients that can (1) protect mitochondrial enzymes and/or stimulate enzyme activity by elevating levels of substrates and cofactors; (2) induce phase-2 enzymes to enhance antioxidant defenses; (3) scavenge free radicals and prevent oxidant production in mitochondria, and (4) repair mitochondrial membrane. Then, we discuss the relationships among mt-nutrient deficiency, mitochondrial decay, and cognitive dysfunction, and summarize available evidence suggesting an effect of mt-nutrient supplementation on AD and PD. It appears that greater effects might be obtained by longer-term administration of combinations of mt-nutrients. Thus, optimal doses of combinations of mt-nutrients to delay and repair mitochondrial decay could be a strategy for preventing and treating cognitive dysfunction, including AD and PD.

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Impaired lipid metabolism in calcium oxalate stone forming rats and DL α - lipoic acid supplementation

1995

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Anticholesterol Activity of α-Lipoic Acid

Cited by 18 publications

References 1 publication

Genetic reduction of lipoic acid synthase expression modestly increases atherosclerosis in male, but not in female, apolipoprotein E-deficient mice

Genetic reduction of lipoic acid synthase expression modestly increases atherosclerosis in male, but not in female, apolipoprotein E-deficient mice

Reducing mitochondrial decay with mitochondrial nutrients to delay and treat cognitive dysfunction, Alzheimer's disease, and Parkinson's disease

Impaired lipid metabolism in calcium oxalate stone forming rats and DL α - lipoic acid supplementation

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