Vitamin E nanoemulsion activity on stored red blood cells

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Red blood cells (RBCs) stored for transfusion purposes undergo a variety of changes, collectively termed RBC storage lesion. Erythrocytes change from discocytic to spherocytic shapes, shed lipids and exhibit decay in ATP content and a decrease in membrane zeta potential due to the loss of glycoprotein sialic acids, which can progressively reduce the ability of the RBCs to resist in circulation (Silva et al., 2012; Bosman, 2013). The loss of RBC deformability is also one of the most commonly observed storage injuries (Fontes et al., 2011; Daly et al., 2014). Deformability is a fundamental erythrocyte mechanical property, allowing RBCs to pass through capillaries with diameters of 2–3 µm, which are smaller than RBC dimensions (6–8 µm). Thus, evaluating and ensuring the overall quality of stored RBCs has become a contentious and relevant issue (Bosman, 2013).
The storage injuries already mentioned, and others, may be directly related to the gradual oxidation of membrane lipids and/or proteins. Deeper knowledge in this area would help to develop new preservative preparations for RBC units, supplemented by antioxidants, which could be capable of improving the biophysical and functional integrity of these cells in circulation after longer storage periods, leading to better post‐transfusion yield (Racek et al., 1997; Chung and Benzie, 2000; Sparrow, 2015).
Over the years, vitamin E has attracted attention as a lipid‐soluble antioxidant, and several studies have demonstrated its activity on lipids by minimising the peroxidation of fatty acids in biological membranes (Racek et al., 1997; Chung and Benzie, 2000; Pfeifer et al., 2008). Vitamin E intercepts hydroxyl and peroxyl radicals, resulting in the formation of tocopheryl radicals, which can even be regenerated by vitamin C (Rucker et al., 2007). Chan et al. (1999) showed that vitamin E supplementation improved clinical symptoms in individuals with haemoglobinopathies, who have increased oxidative stress. Pfeifer et al. (2008) also showed that vitamin E can reduce oxidative stress in RBCs of β‐thalassemia intermedia patients. The role of vitamin C was also investigated to improve the condition of RBCs for transfusion purposes, showing that this antioxidant was able to reduce membrane mechanical fragility and did not alter biochemical parameters in AS‐5 RBC units (Raval et al., 2013). In addition, vitamin C was also able to increase post‐transfusion recovery and decrease alloimmunisation in mice (Stowell et al., 2013).
Therefore, considering that the RBC storage lesion may also be related to lipid oxidation of erythrocyte membranes, this study aimed to evaluate the effect of vitamin E as a possible antioxidant of RBC units stored for transfusion purposes. We believe that this research can provide support for a deeper comprehension of the mechanisms and consequences of vitamin E activity on stored RBCs.
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