Obstructive sleep apnea (OSA) independent of obesity (OBS) imposes severe cardiovascular risk. To what extent plasma cystine concentration (CySS), a novel pro-oxidative vascular risk factor, is increased in OSA with or without OBS is presently unknown. We therefore studied CySS together with the redox state and precursor amino acids of glutathione (GSH) in peripheral blood mononuclear cells (PBMC) in untreated male patients with OSA (apnea-hypopnea-index (AHI) > 15 h, = 28) compared to healthy male controls ( = 25) stratifying for BMI ≥ or < 30 kg m. Fifteen OSA patients were reassessed after 3-5-months CPAP. CySS correlated with cumulative time at an O-saturation <90% (Tu90%) (r = 0.34, < 0.05) beside BMI (r = 0.58, < 0.001) and was higher in subjects with "hypoxic stress" (59.4 ± 2.0 vs. 50.1 ± 2.7 µM, < 0.01) defined as Tu90% ≥ 15.2 min (corresponding to AHI ≥ 15 h). Moreover, CySS significantly correlated with systolic (r = 0.32, < 0.05) and diastolic (r = 0.31, < 0.05) blood pressure. CPAP significantly lowered CySS along with blood pressure at unchanged BMI. Unexpectedly, GSH antioxidant capacity in PBMC was increased with OSA and reversed with CPAP. Plasma CySS levels are increased with OSA-related hypoxic stress and associated with higher blood pressure. CPAP decreases both CySS and blood pressure. The role of CySS in OSA-related vascular endpoints and their prevention by CPAP warrants further studies.
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http://dx.doi.org/10.3390/jcm10071387 | DOI Listing |
RSC Adv
November 2024
Inorganic Chemistry I, Bioinorganic Chemistry, Ruhr University Bochum 44780 Bochum Germany
Since non-thermal atmospheric-pressure ("cold") plasma sources, such as the dielectric-barrier discharge (DBD), have appeared to be remarkably active in wound healing medicine, the elucidation of cold plasma safety and possible secondary undesirable effects becomes of paramount importance. Selenium-containing amino acids, which are commonly incorporated in many enzymes, came in the spotlight for elucidating the plasma impact as easily oxidizable natural targets. The scope of this study was to analyse the impact of non-thermal plasma on selenium-containing amino acids.
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November 2024
Department of Materials Science and Engineering, I-Shou University, Kaohsiung 84001, Taiwan.
B-type natriuretic peptides (BNP) are produced and secreted by the myocardium to reduce blood pressure and cardiac load. They cause vasodilation, natriuresis, growth suppression, and inhibition of the sympathetic nervous system and the renin-angiotensin-aldosterone system. The measurement of plasma BNP levels provides clinically useful information concerning the diagnosis and management of left ventricular dysfunction and heart failure, complementing other diagnostic testing procedures.
View Article and Find Full Text PDFAnal Chem
December 2024
Department of Chemistry, Purdue University, West Lafayette, Indiana 47907, United States.
The biologically important thiols (cysteine, homocysteine, N-acetyl cysteine, and glutathione) are key species in redox homeostasis, and there is a clinical need to measure them rapidly, accurately, and simultaneously at low levels in complex biofluids. The solution to the challenge presented here is based on a new derivatizing reagent that combines a thiol-selective unit to optimize the chemical transformation and a precharged pyridinium unit chosen to maximize sensitivity in mass spectrometry. Derivatization is performed simultaneously with ionization ("reactive ionization"), and mass spectrometry is used to record and characterize the thiol reaction products.
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View Article and Find Full Text PDFFEBS Open Bio
January 2025
Department of Psychiatry, Kagoshima University Graduate School of Medical and Dental Sciences, Japan.
Ferroptosis is a type of programmed cell death owed to an intracellular accumulation of iron resulting in the generation reactive oxygen species, which in turn can cause peroxidation of plasma membrane lipids and ultimately result in cell death. We investigated the potential involvement of VPS13A deficiency in ferroptosis. The VPS13A gene encodes for chorein, and its deficiency is a molecular cause of chorea-acanthocytosis (ChAc), a Huntington-like disease with neurodegeneration in the striatum.
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