Background: Oxidative modification of low-density lipoprotein (LDL) is an important contributor to atherosclerosis. Also, oxidized LDL is suspected to cause accumulation of asymmetric dimethylarginine (ADMA), an endogenous competitive nitric oxide synthase inhibitor, which is suggested to be an independent risk factor for atherosclerosis. This study was performed to evaluate how plasma ADMA is related to plasma nitric oxide production, oxidized LDL and ex vivo susceptibility of LDL to oxidation in mildly hypercholesterolemic otherwise healthy subjects.
Methods: Plasma ADMA was determined using high performance liquid chromatography tandem mass spectrometry. LDL oxidation was estimated by the lag time and rate of copper-induced LDL oxidation. The nitric oxide production in plasma was estimated based on nitrate (NO(3)(-)) determination and plasma oxidized LDL was determined by a capture ELISA.
Results: Low ADMA was a significant determinant for high LDL oxidation rate and concentration of plasma ADMA was associated with nitrate levels.
Conclusions: There may be an interplay between LDL fatty acid oxidation rate and plasma ADMA and nitrate. We hypothesize that plasma ADMA has a bivalent role: high ADMA may have a protective role in decelerating LDL fatty acid oxidation and also a risk factor for endothelial dysfunction by decreasing availability of nitric oxide.
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http://dx.doi.org/10.1016/j.cca.2006.02.028 | DOI Listing |
Nitric Oxide
December 2024
Maj Institute of Pharmacology Polish Academy of Sciences, 12 Smetna Street, 31-343, Krakow, Poland. Electronic address:
l-arginine derivatives (ADMA, SDMA, NMMA) are endogenous inhibitors of nitric oxide (NO֗) production, which is essential in critical brain processes including blood-brain barrier (BBB) integrity and long-term potentiation (LTP). ADMA and NMMA are degraded by dimethylarginine dimethylaminohydrolase 1 (DDAH1) and protein arginine methyltransferase 5 (PRMT5) is an emerging epigenetic enzyme that mainly represses transcription of target genes via symmetric dimethylation of arginine residues. There is no data concerning the impact of metabotropic glutamate receptors (mGlu) ligands on this aspect of brain physiology.
View Article and Find Full Text PDFBiochimie
November 2024
Unitat de Medicina Preventiva, ANUT-DSM, Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Reus, (FMCS URV), Spain; IISPV, Areas of Family and Community Medicine, Spain; CIBERobn ISCIII, Spain. Electronic address:
PLoS One
October 2024
Pharmaceutical Sciences Research Division, King's College London, London, United Kingdom.
L-Arginine is the physiological substrate for the nitric oxide synthase (NOS) family, which synthesises nitric oxide (NO) in endothelial and neuronal cells. NO synthesis can be inhibited by endogenous asymmetric dimethylarginine (ADMA). NO has explicit roles in cellular signalling and vasodilation.
View Article and Find Full Text PDFAm J Hypertens
October 2024
Department of Women's and Children's Health, Section of Obstetrics and Gynecology, Uppsala University, Uppsala, Sweden.
Nutr Metab Cardiovasc Dis
August 2024
School of Public Health, Suzhou Medical College of Soochow University, Suzhou, China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-communicable Diseases, Suzhou Medical College of Soochow University, Suzhou, China; MOE Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China. Electronic address:
Background And Aims: Previous studies have linked aberrant nitric oxide (NO) metabolism with vascular diseases. Although arginine, homoarginine, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA) are involved in NO metabolic pathways, their associations with ischemic stroke (IS) remain unclear.
Methods And Results: We conducted a case-control study nested within the Prospective Follow-up Study on Cardiovascular Morbidity and Mortality in China (PFS-CMMC) (2013-2018, n = 16,457; median follow-up time: 5.
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