L-Carnitine hydrochloride
(Synonyms: L-肉毒碱盐酸盐; (R)-Carnitine hydrochloride; Levocarnitine hydrochloride) 目录号 : GC38920L-Carnitine ((R)-Carnitine, Levocarnitine) hydrochloride improves oxygen saturation, and inhibits leukotriene synthesis. L-Carnitine hydrochloride functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation.
Cas No.:6645-46-1
Sample solution is provided at 25 µL, 10mM.
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L-Carnitine ((R)-Carnitine, Levocarnitine) hydrochloride improves oxygen saturation, and inhibits leukotriene synthesis. L-Carnitine hydrochloride functions to transport long chain fatty acyl-CoAs into the mitochondria for degradation by β-oxidation.
[1] Nevin Uzuner, et al. Acta Med Okayama. 2002 Dec;56(6):295-301. [2] Gustavo C Ferreira, Mary C McKenna. Neurochem Res. 2017 Jun;42(6):1661-1675.
Cas No. | 6645-46-1 | SDF | |
别名 | L-肉毒碱盐酸盐; (R)-Carnitine hydrochloride; Levocarnitine hydrochloride | ||
Canonical SMILES | C[N+](C)(C)C[C@H](O)CC(O)=O.[Cl-] | ||
分子式 | C7H16ClNO3 | 分子量 | 197.66 |
溶解度 | Water: 250 mg/mL (1264.80 mM) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 5.0592 mL | 25.296 mL | 50.5919 mL |
5 mM | 1.0118 mL | 5.0592 mL | 10.1184 mL |
10 mM | 0.5059 mL | 2.5296 mL | 5.0592 mL |
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L-carnitine exposure and mitochondrial function in human neuronal cells
Neurochem Res 2013 Nov;38(11):2336-41.PMID:24005823DOI:10.1007/s11064-013-1144-7.
L-Carnitine is a naturally occurring substance required in mammalian energy metabolism that functions by facilitating long-chain fatty acid entry into cellular mitochondria, thereby delivering substrate for oxidation and subsequent energy production. It has been purposed that L-carnitine may improve and preserve cognitive performance, and may lead to better cognitive aging through the life span, and several controlled human clinical trials with L-carnitine support the hypothesis that this substance has the ability to improve cognitive function. We further hypothesized that, since L-carnitine is an important co-factor of mammalian mitochondrial energy metabolism, acute administration of L-carnitine to human tissue culture cells should result in detectable increases in mitochondrial function. Cultures of SH-SY-5Y human neuroblastoma and 1321N1 human astrocytoma cells grown in 96-well cell culture plates were acutely administered L-Carnitine hydrochloride, and then, mitochondrial function was assayed using the colorimetric 2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxyanilide inner salt cell assay kit in a VERSAmax tunable microplate reader. Significant increases in mitochondrial function were observed when human neuroblastoma or human astrocytoma cells were exposed to 100 nM (20 μg L-Carnitine hydrochloride/L) to 100 μM (20 mg L-Carnitine hydrochloride/L) concentrations of L-Carnitine hydrochloride in comparison to unexposed cells, whereas no significant positive effects were observed at lower or higher concentrations of L-Carnitine hydrochloride. The results of the present study provide insights for how L-carnitine therapy may significantly improve human neuronal function, but we recommend that future studies further explore different derivatives of L-carnitine compounds in different in vitro cell-based systems using different markers of mitochondrial function.
Protective effect of L-carnitine on renal ischaemia-reperfusion injury in the rat
Cell Biochem Funct 2005 May-Jun;23(3):151-5.PMID:15386530DOI:10.1002/cbf.1159.
This study was designed to investigate the effect of L-carnitine in ischaemia and reperfusion of the rat kidney. Rats were randomly allocated into three groups. Group I (control group; n = 6) received no treatment. Group II (isotonic saline group; n = 6), received 2 ml of isotonic saline 15 min before the renal ischaemia, and group III (carnitine group; n = 6) received L-Carnitine hydrochloride (100 mg kg(-1)) intraperitoneally. At the end of the reperfusion period, rats were sacrificed. Tissue malondialdehyde level (MDA), myeloperoxidase (MPO) activity, and nitrite/nitrate (NO) level of renal tissue were measured to evaluate the lipid peroxidation, neutrophil function, and nitric oxide metabolism, respectively. The tissue levels of MDA, MPO and NO were lower in group III (71.8 +/- 8.4, 172.1 +/- 27.4 U g(-1) tissue, 76.3 +/- 29.7 micromol l(-1) respectively) than levels in groups I (103.4 +/- 13.4 nmol g(-1), 325.9 +/- 20.2 U g(-1) tissue, 144.5 +/- 39.2 micromol l(-1), respectively) and II (103.5 +/- 11.4 nmol g(-1), 317.1 +/- 41.5 U g(-1) tissue, 148.9 +/- 23.9 micromol l(-1), respectively). It is shown that carnitine protects kidney tissue against ischaemia-reperfusion injury.