期刊
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
卷 129, 期 -, 页码 25-29出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2022.09.004
关键词
Nitric oxide; Nitrite; Red blood cell deformability; Diet; Exercise; Oxidative stress; Redox; Microcirculation
The rheological properties of red blood cells (RBCs) are important for their microcirculation. Lifestyle-related diseases can lead to decreased RBC deformability, which is associated with increased oxidative stress and decreased nitric oxide (NO) bioavailability. NO can protect RBC membrane flexibility by shielding redox-sensitive cysteine residues. Nitrate-rich diets and moderate exercise can enhance NO production and increase RBC deformability. This review focuses on the molecular mechanism of NO generation and its prophylactic effects against decreased RBC deformability in lifestyle-related diseases.
The rheological properties of red blood cells (RBCs) play an important role in their microcirculation. RBCs can elastically deform in response to mechanical forces to pass through narrow vessels for effective gas exchange in peripheral tissues. Decreased RBC deformability is observed in lifestyle-related diseases such as diabetes mellitus, hypercholesterolemia, and hypertension, which are pathological conditions linked to increased oxidative stress and decreased nitric oxide (NO) bioavailability. Redox-sensitive cysteine residues on RBC cytoskeletal proteins, such as alpha-and beta-spectrins, responsible for membrane flexibility, are affected by prolonged oxidative stress, leading to reversible and irreversible oxidative modifications and decreased RBC deformability. However, endogenously, and exogenously generated NO protects RBC membrane flexibility from further oxidative modi-fication by shielding redox-sensitive cysteine residues with a glutathione cap. Recent studies have shown that nitrate-rich diets and moderate exercise can enhance NO production to increase RBC deformability by increasing the interplay between RBCs and vascular endothelium-mediated NO bioavailability for microcirculation. This review focuses on the molecular mechanism of RBC-and non-RBC-mediated NO generation, and how diet-and exercise-derived NO exert prophylactic effects against decreased RBC deformability in lifestyle-related diseases with vascular endothelial dysfunction.
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