Arsenic (As) is a toxic semi-metal of wide distribution in nature. People living in regions where drinking water contains large quantities of arsenic, have an unusually high likelihood of developing blood-vessel diseases, but little is known about the mechanisms involved, i.e. the blood rheologic alterations that would contribute to the circulatory obstruction. Erythrocytes are the main target cells for arsenic compounds systemically absorbed and their cell membrane is the first place against the toxic. In this paper we have examined the in vitro effect of arsenic (As V ) on the rheologic properties of human erythrocytes in relation with membrane fluidity and internal microviscosity. According to our present results, As V treatment produces oxidative degradation of membrane lipids and alteration of internal microviscosity. These red blood cells (RBCs) membrane and cytoplasmic structural damage consequently alters RBCs rheologic properties: an alteration of the RBCs discoid shape to stomatocytes, a diminution of erythrocyte deformability and an enhancement of osmotic fragility and cell aggregability. These effects impaired blood fluid behaviour that contribute to obstruct peripheral circulation and provides anemia, both clinic evidences typical of arsenic cronic intoxication.
The link between aluminium (Al(III)) and a range of disorders in organisms (plants and animals including human beings) has been stated in diverse studies. As regards as human beings in particular, there are numerous studies on this metal's toxicity in relation to pathological processes. Only few references to the metal's effect upon cell rheological properties can be found. In this study, we present evidence for alterations in the rheological properties of cells as consequence of the Al(III)'s interaction with human red blood cell membrane. Al(III) could damage membrane functions of the red blood cell by favouring lipid peroxidation reactions due to the presence of Fe(II) as an initiator. The metal's effect on lipid bilayer, and probably on the cytoskeleton as well, would constitute the cause for the impaired erythrocyte rheology.
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