“…Thus, the observed in vitro binding of Cd 2+ , Hg 2+ and CH 3 Hg + to RBC cytosol constituents (i.e., GSH, Hb and other proteins) helps to explain changes in the redox status of the RBCs from fishermen, which, in turn, are implicated in the observed increased prevalence of hypertension and type 2 diabetes (among the 55 fishermen, 34% exhibited hypertension and 11% type 2 diabetes, while in the control group of 25, the corresponding values were 24% and 0%, respectively) [ 100 , 101 ]. Related to these findings, jewelry workers who were occupationally exposed to Cd also exhibited an increased RBC fragility and oxidative stress [ 102 ] and red-backed voles living in the vicinity of a metal smelter exhibited similar RBC aberrations [ 103 ], clearly demonstrating a need to better understand how bioinorganic chemistry processes of toxic metal(loid) species that unfold in the RBC cytosol cumulatively affect their stability and, thus, the hematological system in more general terms [ 104 ]. Closely related to this, it was recently observed that the Zn-metalloprotein carbonic anhydrase I (CA), after it is released from RBCs following their rupture, does not appear to bind to any plasma proteins [ 105 ], implicating CA in mediating adverse processes that unfold in the cells that make up the endothelium of blood vessels and are therefore linked to the etiology of atherosclerosis [ 106 ].…”