Comparison of the Effects of l‐Carnitine and Acetyl‐l‐Carnitine on Carnitine Levels, Ambulatory Activity, and Oxidative Stress Biomarkers in the Brain of Old Rats
Department of Molecular and Cell Biology, Uniersity of California, Berkeley, CA 94720, USA. Annals of the New York Academy of Sciences
(Impact Factor: 4.38).
12/2004; 1033(1):117-31. DOI: 10.1196/annals.1320.011
L-carnitine and acetyl-L-carnitine (ALC) are both used to improve mitochondrial function. Although it has been argued that ALC is better than l-carnitine in absorption and activity, there has been no experiment to compare the two compounds at the same dose. In the present experiment, the effects of ALC and L-carnitine on the levels of free, acyl, and total L-carnitine in plasma and brain, rat ambulatory activity, and biomarkers of oxidative stress are investigated. Aged rats (23 months old) were given ALC or L-carnitine at 0.15% in drinking water for 4 weeks. L-carnitine and ALC were similar in elevating carnitine levels in plasma and brain. Both increased ambulatory activity similarly. However, ALC decreased the lipid peroxidation (malondialdehyde, MDA) in the old rat brain, while L-carnitine did not. ALC decreased the extent of oxidized nucleotides (oxo8dG/oxo8G) immunostaining in the hippocampal CA1 and cortex, while L-carnitine did not. ALC decreased nitrotyrosine immunostaining in the hippocampal CA1 and white matter, while L-carnitine did not. In conclusion, ALC and L-carnitine were similar in increasing ambulatory activity in old rats and elevating carnitine levels in blood and brain. However, ALC was effective, unlike L-carnitine, in decreasing oxidative damage, including MDA, oxo8dG/oxo8G, and nitrotyrosine, in old rat brain. These data suggest that ALC may be a better dietary supplement than L-carnitine.
Available from: Chidiebere Uchendu
- "Acetyl-L-carnitine (ALC) is a potent antioxidant that is widely distributed in the mammalian brain where it is involved in the regulation of carbohydrate, lipid, and protein metabolism (Picconi et al. 2006). ALC may act as an antioxidant either having a primary antioxidant activity (inhibiting free radical (FR) generation, scavenging the initiating FR, and terminating their propagation reaction) or more likely functioning as a secondary antioxidant (repairing oxidized polyunsaturated fatty acid esterified in membrane phospholipids ) (Liu et al. 2004). Considering all these, therefore, the present paper investigated the beneficial effect of ALC on alterations of lipid profiles and oxidative stress parameters induced by CPF in Wistar rats. "
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ABSTRACT: The present study evaluated the beneficial effect of acetyl-L-carnitine (ALC) on subacute chlorpyrifos (CPF)-induced alterations in serum lipid profiles and some biomarkers of oxidative stress in Wistar rats. Twenty-eight adult male rats divided into four groups of seven animals each (group I–IV) were used: I (S/oil) received soya oil (2 ml kg−1), II (ALC) received ALC (300 mg kg−1); III (CPF) received CPF (8.5 mg kg−1 ∼ 1/10th LD50); IV (ALC+CPF) was pretreated with ALC (300 mg kg−1) and then exposed to CPF (8.5 mg kg−1), 30 min later. The treatment was orally for 28 days duration. Sera obtained from blood samples were evaluated for the levels of triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-c), malondialdehyde (MDA), and the activities of superoxide dismutase (SOD) and catalase (CAT). The levels of low density lipoprotein-cholesterol (LDL-c), very low density lipoprotein-cholesterol (VLDL-c), and atherogenic index (AI) were calculated. The result showed that elevated levels of TG, TC, LDL-c, VLDL-c, AI, and MDA, and the decreased levels of HDL-c, CAT, and SOD induced by CPF were modulated by ALC. It was concluded that ALC ameliorated the alterations in serum lipid and oxidative stress induced by CPF exposure in the rats, partly through its antioxidant properties.
Available from: Azam Yousefi
- "The syndrome has been observed worldwide but the incidence is more dramatic in broilers reared at high altitudes (Khajali et al., 2007). L-carnitine (β-hydroxy-γ-N-trimethylaminobutyric acid) is a quaternary ammonium compound with several cellular functions including the role in the transport of long-chain fatty acids into the mitochondrial matrix for oxidation to provide cellular energy (Arslan, 2006), the modulation of the cellular and especially intra-mitochondrial acyl-CoA:CoA ratio (Tanphaichitr and Leelahagul, 1993), the participation in scavenging reactive oxygen species (Liu et al., 2004), and immunomodulatory effect (Buyse et al., 2007). L-carnitine enhances myocardial function by improving fatty acid transport into the mitochondria (Ueland et al., 2012). "
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ABSTRACT: The present study was conducted to examine the effects of L-carnitine on pulmonary hypertensive response in broiler chickens reared at high altitude and exposed to hypobaric hypoxia. A total of 192 day-old male broilers (Cobb 500) were randomly assigned to 4 treatments and 4 replicates of 12 chicks. A basal diet composed of mainly corn and soybean meal was formulated and served as a control. Three additional treatments were made by supplementing graded levels of L-carnitine (50, 100, and 150 mg/kg). Chicks received dietary treatments at free access from 1 to 42 days of age. Results indicated that feeding L-carnitine at 100 mg/kg caused a significant increase in plasma nitric oxide (NO) with concomitant decrease in plasma malonedialdehyde (MDA). The Lead II electrocardiogram indicated reductions of S wave amplitude for all three doses of L-carnitine relative to the control and the difference between the birds that received L-carnitine at 50 mg/kg and the control was significant (P＜0.05). The right ventricular weight ratio (RV/TV) tended to decline when L-carnitine supplemented to diets. In conclusion, L-carnitine reduced ascites mortality in broiler chickens by increased NO production, reduced MDA concentration, and reduced right ventricular hypertrophy.
Available from: Gjumrakch Aliev
- "In contrast, neurons obtained from aged control groups showed a series of mitochondrial abnormalities, such as the presence of giant mitochondria and mitochondria with partial or complete damaged cristae. Targeting mitochondrial OS improved the overall cognitive ability of aged rats [148,149,150,152,157,162] and aged dogs . "
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ABSTRACT: Mitochondrial dysfunction may be a principal underlying event in aging, including age-associated brain degeneration. Mitochondria provide energy for basic metabolic processes. Their decay with age impairs cellular metabolism and leads to a decline of cellular function. Alzheimer disease (AD) and cerebrovascular accidents (CVAs) are two leading causes of age-related dementia. Increasing evidence strongly supports the theory that oxidative stress, largely due to reactive oxygen species (ROS), induces mitochondrial damage, which arises from chronic hypoperfusion and is primarily responsible for the pathogenesis that underlies both disease processes. Mitochondrial membrane potential, respiratory control ratios and cellular oxygen consumption decline with age and correlate with increased oxidant production. The sustained hypoperfusion and oxidative stress in brain tissues can stimulate the expression of nitric oxide synthases (NOSs) and brain endothelium probably increase the accumulation of oxidative stress products, which therefore contributes to blood brain barrier (BBB) breakdown and brain parenchymal cell damage. Determining the mechanisms behind these imbalances may provide crucial information in the development of new, more effective therapies for stroke and AD patients in the near future.
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