Enhancement of Platelet Aggregation and Thrombus Formation by Arsenic in Drinking Water: A Contributing Factor to Cardiovascular Disease

Cardiovascular effects of arsenic: clinical and epidemiological findings

“…As appears to enhance platelet aggregation (Lee et al 2002), possibly by exposing phosphatidylserine (Bae et al 2009) though studies are conflicting (Lin et al 2010), and reduces endothelial fibrinolytic activity by reducing t-PA and increasing PAI-1 level and activity (Jiang et al 2002), and reduces synthesis of proteoglycans such as heparan sulfate (Fujiwara et al 2005). The activity of As on coagulation and platelets could aggravate thrombosis when the atherosclerotic plaque ruptures (Fig.…”

Protein binding interaction of warfarin and acetaminophen in presence of arsenic and of the biological system

“…The EPA also recently proposed to reduce its drinking water standard from 50 to 10 ppb; however, this newly proposed maximum contaminant level is now being reevaluated for scientific merit (Kaiser, 2001). Arsenic ingestion may also aggravate the platelet aggregation and may cause induce vascular diseases (Lee et al, 2002). The activation and resulting aggregation of platelets are believed to be important events in both hemostasis and the pathogenesis of various vascular diseases due to thrombus formation (Marcus and Safier, 1993).…”

Update onarsenic Exposure Link inCancer

“…This ATP formation in Glycolysis is inhibited while bypassing the phosphoglycerate kinase (Moreover, the formation of2,3-bisphosphoglycerate in erythrocytes might be affected, followed by a higher oxygen affinity of hemoglobin and subsequently enhanced cyanosis).As shown by Gresser(1981),sub mitochondrial particles synthesize adenosine-5 ' -diphosphate-arsenate from ADP and arsenate in presence of succinate. Thus, by a variety of mechanisms arsenate leads to an impairment of cell respiration and subsequently diminished ATP formation [41].Experiments demonstrated enhanced arterial thrombosis in rat animal model, elevation of serotonin levels, thromboxane A [2] and adhesion proteins in platelets, while human platelets showed similar responses [42].The effect on vascular endothelium may eventually be mediated by arsenicinduced formation of nitric oxide. It was demonstrated that +3 As concentrations substantially lower than concentrations required for inhibition of lysosomal protease cathepsin L in B cell line TA3 were sufficient to trigger apoptosis in same B cell line, while latter could be mediating immunosuppressive effects [43].…”