Arsenic intoxication, a hemorheologic view

Abstract

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.

Chronic arsenic intoxication diagnostic score (CAsIDS)

“…Anemia – including hemolytic, poikilocytic and megaloblastic anemia – has been frequently observed in environmental, nutritional, iatrogenic, osteoresorptive as well as experimental arsenic intoxication (Biswas, Sen, & Biswas, ; Bollini et al, ; Correia et al, ; Dani, ; Heck et al, ; Hopenhayn, Bush, Bingcang, & Hertz‐Picciotto, ; Lee et al, ; Westhoff, Samaha, & Barnes, ). Arsenite causes extensive damage to red blood cells, which impairs their antioxidant system and alters the major cellular metabolic pathways (Maheshwari, Khan, & Mahmood, ).…”

“…Anemiaincluding hemolytic, poikilocytic and megaloblastic anemiahas been frequently observed in environmental, nutritional, iatrogenic, osteoresorptive as well as experimental arsenic intoxication (Biswas, Sen, & Biswas, 2010;Bollini et al, 2010;Correia et al, 2009;Dani, 2013;Heck et al, 2008;Hopenhayn, Bush, Bingcang, & Hertz-Picciotto, 2006;Lee et al, 2004;Westhoff, Samaha, & Barnes, 1975).…”

Gallic acid and MiADMSA reversed arsenic induced oxidative/nitrosative damage in rat red blood cells

“…Arsenic itself and its metabolites possess high haemoglobin (Hb) binding affinity and thus eventually accumulate in blood [32]. Arsenic causes membrane and cytoplasmic damage to RBC resulting in morphological changes in RBC from discoid shape to stomatocytes, decrease in deformability, increase in osmotic fragility and cell agreeability [33]. The above all factors contribute for the elimination of damaged cells from blood circulation and impairs oxygen delivery.…”

Hydroxyurea‐induced stomatocytes in a patient presenting with polycythemia vera

“…When associated to macrocytosis, a myelodysplastic syndrome/neoplasm should be ruled out. A few drugs have been associated with the occurrence of stomatocytes, in vitro or in vivo: neurotropic drugs (chlorpromazine, diazepam, citalopram) [4,5] or arsenic [6].Here, we report the case of an 80-year-old man, without previous history of hemolytic anemia or liver dysfunction, who was diagnosed with a JAK2 V617F negative-polycythemia vera requiring a treatment with hydroxyurea 500 mg twice daily. At diagnosis, blood count was Hb 21 g/dL, Ht 0.62, MCV 98 fL, MCH 32 pg, without any special comment on red cells morphology.…”

“…When associated to macrocytosis, a myelodysplastic syndrome/neoplasm should be ruled out. A few drugs have been associated with the occurrence of stomatocytes, in vitro or in vivo: neurotropic drugs (chlorpromazine, diazepam, citalopram) [4,5] or arsenic [6].…”