Browsing by Subject "Red blood cells"
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Publication Association between vitamin D status and eryptosis - results from the German National Cohort Study(2023) Ewendt, Franz; Schmitt, Marvin; Kluttig, Alexander; Kühn, Julia; Hirche, Frank; Kraus, Frank B.; Ludwig-Kraus, Beatrice; Mikolajczyk, Rafael; Wätjen, Wim; Bürkner, Paul-Christian; Föller, Michael; Stangl, Gabriele I.; Ewendt, Franz; Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany; Schmitt, Marvin; Cluster of Excellence SimTech, University of Stuttgart, Stuttgart, Germany; Kluttig, Alexander; Institute of Medical Epidemiology, Biostatistics, and Informatics, Medical Faculty of the Martin Luther University Halle-Wittenberg, Halle (Saale), Germany; Kühn, Julia; Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany; Hirche, Frank; Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany; Kraus, Frank B.; Central Laboratory, Department of Laboratory Medicine, University Hospital Halle, Halle (Saale), Germany; Ludwig-Kraus, Beatrice; Central Laboratory, Department of Laboratory Medicine, University Hospital Halle, Halle (Saale), Germany; Mikolajczyk, Rafael; Institute of Medical Epidemiology, Biostatistics, and Informatics, Medical Faculty of the Martin Luther University Halle-Wittenberg, Halle (Saale), Germany; Wätjen, Wim; Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), Germany; Bürkner, Paul-Christian; Cluster of Excellence SimTech, University of Stuttgart, Stuttgart, Germany; Föller, Michael; Department of Physiology, University of Hohenheim, Stuttgart, Germany; Stangl, Gabriele I.; Institute of Agricultural and Nutritional Sciences, Martin Luther University Halle-Wittenberg, Halle (Saale), GermanyVitamin D, besides its classical effect on mineral homeostasis and bone remodeling, can also modulate apoptosis. A special form of apoptosis termed eryptosis appears in erythrocytes. Eryptosis is characterized by cell shrinkage, membrane blebbing, and cell membrane phospholipid disorganization and associated with diseases such as sepsis, malaria or iron deficiency, and impaired microcirculation. To our knowledge, this is the first study that linked vitamin D with eryptosis in humans. This exploratory cross-sectional trial investigated the association between the vitamin D status assessed by the concentration of plasma 25-hydroxyvitamin D (25(OH)D) and eryptosis. Plasma 25(OH)D was analyzed by LC–MS/MS, and eryptosis was estimated from annexin V-FITC-binding erythrocytes by FACS analysis in 2074 blood samples from participants of the German National Cohort Study. We observed a weak but clear correlation between low vitamin D status and increased eryptosis ( r = − 0.15; 95% CI [− 0.19, − 0.10]). There were no differences in plasma concentrations of 25(OH)D and eryptosis between male and female subjects. This finding raises questions of the importance of vitamin D status for eryptosis in terms of increased risk for anemia or cardiovascular events.Publication GLUT-1 content and interaction with stomatin in red blood cells from species without vitamin C biosynthesis and their relevance for diabetes mellitus type 1(2016) Frey, Tabea Caroline; Biesalski, Hans-KonradAscorbic acid is commonly known as vitamin C. By definition, vitamins, with the exception of vitamin D, are substances which can not be synthesized, but are essential for the organism. In this light, vitamin C is special. It is hypothesized that millions of years ago some species, like primates, Guinea pigs and fruit bats, lost the ability to synthesize ascorbate from glucose due to an inactivation of an enzyme called L-gulono-g-lactone oxidase. Since then, these species have been dependent on dietary intake of this micronutrient. Ascorbate is not only the most efficient watersoluble antioxidant, but also an important cofactor in neurotransmitter or collagen biosynthesis. An inadequate intake of this vitamin leads to scurvy. In 2008, a French researcher documented that all species that lost the ability to synthesize ascorbic acid express a different facilitative glucose transporter isoform(GLUT) in their erythrocytes. The expressed GLUT-1 transports not only glucose but also dehydroascorbate which is the oxidized form of vitamin C. Was that different GLUT expression the keystone event for the evolutionary success of these species? To examine the questions regarding the evolutionary benefit of this transporter expression, the kinetics of ascorbate and dehydroascorbate transport into erythrocytes from four different species were evaluated. Further, recycling and disposal of the transported vitamin as well as a possible accumulation were observed. The results demonstrate that there are three different transport types of dehydroascorbate. One which does not transport the vitamin at all, one whose transport of dehydroascorbate competes with glucose and one which absorbs dehydroascorbate completely independent of the extracellular glucose concentration. After absorption, vitamin C is not recycled and is not disposed back into the extracellular fluid. Additionally, it is not stored in the cell until the erythrocyte undergoes apoptosis. The evolutionary benefit is found in an electron transfer across the erythrocyte membrane from intracellular ascorbate to the extracellular, oxidized form of vitamin C. In an energetic light, this recycling of extracellular vitamin C is more efficient than the de novo synthesis of the micronutrient. Therefore, the erythrocyte acts not as a reservoir for vitamin C storage, but as a reservoir for electron storage to prevent degradation and loss of dehydroascorbate in times of high oxidative stress. This electron reservoir becomes more important in diseases with high levels of oxidative stress. A metabolic disorder, which is frequently described to be accompanied by high levels of oxidative stress and lowered vitamin C levels in plasma and cells, is Diabetes mellitus. The decreased plasma concentrations do not result from a smaller dietary intake. Probably, the uptake of dehydroascorbate into erythrocytes, and, therefore, the extracellular ascorbate recycling is disordered. Investigations of the distribution of GLUT-1 in different erythrocyte membrane subdomains showed that the regulation of this transporter is altered in subjects with diabetes mellitus type 1 compared to healthy controls. In vitro, no differences in dehydroascorbate transport rate could be observed, but significantly decreased intra-erythrocyte vitamin C concentrations were detected in vivo. In conclusion, the altered regulation of GLUT-1 in the erythrocyte membrane in the case of diabetes can affect vitamin C recycling in plasma. A decreased ascorbate pool in the cells leads to a decreased recycling capacity, and, therefore, to a lower antioxidant defense outside the cell. Due to that knowledge, the recommended dietary intake of vitamin C in the case of diabetes mellitus must be reconsidered to prevent further complications.