History of L-carnitine: Implications for renal disease

Matera, M; Bellinghieri, Guido; Costantino, Giuseppe; Santoro, Domenico; Calvani, Menotti; Savica, Vincenzo

doi:10.1053/jren.2003.50010

Cited by 58 publications

(45 citation statements)

References 70 publications

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“…[24,25] Most of these symptoms were found to be improved by L-carnitine administration. [25][26][27] Catechins are a group of flavonoidspresent in vegetables and plant-derived beverages and food, like tea and chocolate-that have attracted particular attention due to their relative high antioxidant capacity and free radical scavenging activities in biological systems. [28][29][30] Owing to the multiple complications caused by oxidative stress and inflammatory response associated with disordered L-arginine-NO pathway and deficient anti-oxidant defense mechanisms in CRF.…”

Section: Aa Korishmentioning

confidence: 99%

Multiple Antioxidants and L-Arginine Modulate Inflammation and Dyslipidemia in Chronic Renal Failure Rats

Korish

2010

Renal Failure

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The kidney is an important source of L-arginine, the endogenous precursor of nitric oxide (NO). Surgical problems requiring extensive renal mass reduction (RMR) decrease renal NO production, leading to multiple hemodynamic and homeostatic disorders manifested by hypertension, oxidative stress, and increased inflammatory cytokines. Using the RMR model of chronic renal failure (CRF), we assessed the effects of twelve weeks' administration of L-arginine and/or a mixture of antioxidants (L-carnitine, catechin, vitamins E and C) on plasma cytokines, soluble intercellular adhesion molecule-1 (sICAM-1), nitrate and nitrites (NO 2 /NO 3 ), lipid profile, blood pressure, and renal function. CRF rats showed increased plasma IL-1a, IL1-b, IL-6, TNF-a, and sICAM-1 levels and decreased anti-inflammatory cytokines IL-4 and 10 levels, hypertension, and dyslipidemia. L-arginine treatment improved kidney functions, decreased systolic blood pressure, and decreased inflammatory cytokines levels. Antioxidants administration decreased inflammatory cytokines and sICAM-1 levels and increased IL-4 levels. Combined use of both L-arginine and the antioxidant mixture were very effective in their tendency to recover normal values of kidney functions, plasma cytokines, sICAM-1, blood pressure, NO 2 /NO 3 , cholesterol, and triglycerides concentrations. Indeed, the effects of L-arginine and the antioxidants on the reduction of proinflammatory cytokines may open new perspectives in the treatment of uremia.

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Section: Aa Korishmentioning

confidence: 99%

Multiple Antioxidants and L-Arginine Modulate Inflammation and Dyslipidemia in Chronic Renal Failure Rats

Korish

2010

Renal Failure

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“…Myristic acid exhibited a protective effect on renal necrosis in rats fed a methyl-deficient diet; however, it should be investigated whether the level of myristic acid in the uremic patient serum increased as a metabolic compensation for uremia-related pathological variations. Numerous studies have reported that carnitine plays an indispensable role in the oxidation and metabolism of fatty acids, thus, the lineloic acid and myristic acid disorders observed in uremic patient sera probably reflect the depletion of carnitine [28], which has significant consequences for patients with myocardial diseases and kidney failure.…”

Section: Clinical Applicationmentioning

confidence: 99%

GC-MS with ethyl chloroformate derivatization for comprehensive analysis of metabolites in serum and its application to human uremia

et al. 2008

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Abstract:An optimized method based on GC-MS with ethyl chloroformate derivatization has been developed for the comprehensive analysis of endogenous metabolites in serum. Twenty-two reference standards and serum samples were used to validate the proposed method. The correlation coefficient was higher than 0.9900 for each of the standards, and the LOD varied from 125 to 300 pg on-column. The analytical equipment exhibited good repeatability (RSD<10%) for all of the standards. Both the repeatability and the within-48-h stability of the analytical method were satisfactory (RSD<10%) for the 18 metabolites identified in the serum samples. Mean recovery was acceptable for the 18 metabolites, ranging from 70% to 120% with RSDs of less than 10%. Using the optimized protocol and a subsequent multivariate statistical technique, complete differentiation was achieved between the metabolic profile of uremic patients and that of age-and sex-matched normal subjects. Significantly decreased levels of valine, leucine, and isoleucine and increased levels of myristic acid and linoleic acid were observed in the patient group. This work demonstrated that this method is suitable for serumbased metabolic profiling studies.

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“…The main functions of L -carnitine [3-hydroxy-4-(trimethylazaniumyl)butanoate] include transferring the long-chain fatty acids through the mitochondrial barrier, the protection of membrane structures and the reduction of lactate production [8]. Lipid metabolism disorder in ischemia and anoxia can lead to accumulation of fatty acyl-CoA, which in turn may lead to membrane structure damage and cell death [9,10].…”

Section: Introductionmentioning

confidence: 99%

Effects of <smlcap>L</smlcap>-Carnitine on High Glucose-Induced Oxidative Stress in Retinal Ganglion Cells

Cao

Shi

et al. 2014

Pharmacology

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Background: Oxidative stress plays a role in diabetic retinopathy. L-Carnitine is an endogenous mitochondrial membrane compound. Objective: To elucidate the protective effects of L-carnitine on high glucose-induced oxidative stress in retinal ganglion cells (RGCs). Methods: Hoechst 33258 staining was used to estimate cell loss. Mitochondrial function was predicted by mitochondrial membrane potential (ΔΨm) measurement. The expression of apoptosis-related protein was measured by Western blotting. Assays for reactive oxygen species (ROS) accumulation, lipid peroxidation, total antioxidative capacity (T-AOC) and antioxidant defense enzymes were completed to explain the antioxidative capacity of L-carnitine. Results:L-Carnitine (12 h) inhibited high glucose-mediated cell loss and restored mitochondrial function including a reversion of ΔΨm loss and cytochrome c release. Cell apoptosis triggered by high glucose was also inhibited by L-carnitine, characterized by the downregulation of caspase-9, caspase-3 and Bax/Bcl-2. Furthermore, L-carnitine inhibited high glucose-induced ROS production and lipid peroxidation and promoted endogenous antioxidant defense components including superoxide dismutase, glutathione peroxidase, catalase and T-AOC in a concentration-dependent manner. Conclusions:L-Carnitine may protect RGCs from high glucose-induced injury through the inhibition of oxidative damage, mitochondrial dysfunction and, ultimately, cell apoptosis.

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History of L-carnitine: Implications for renal disease

Cited by 58 publications

References 70 publications

Multiple Antioxidants and L-Arginine Modulate Inflammation and Dyslipidemia in Chronic Renal Failure Rats

Multiple Antioxidants and L-Arginine Modulate Inflammation and Dyslipidemia in Chronic Renal Failure Rats

GC-MS with ethyl chloroformate derivatization for comprehensive analysis of metabolites in serum and its application to human uremia

Effects of <smlcap>L</smlcap>-Carnitine on High Glucose-Induced Oxidative Stress in Retinal Ganglion Cells

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