Abstract
The objective of this investigation was to evaluate postmortem changes of electric charge of human erythrocytes and thrombocytes after fatal carbon monoxide (CO) poisoning. The surface charge density values were determined on the basis of the electrophoretic mobility measurements of the cells carried out at various pH values of electrolyte solution. The surface charge of erythrocyte membranes after fatal CO poisoning as well as after sudden unexpected death increased compared to the control group in the whole range of experimental pH values. Also, a slight shift of the isoelectric point of erythrocyte membranes to high pH values was observed. The surface charge of thrombocyte membranes after fatal CO poisoning decreased at low pH compared to the control group. However, at high pH, the values increased compared to the control group. The isoelectric point of thrombocyte membranes after fatal CO poisoning was considerably shifted toward low pH values compared to the control group. The observed changes are probably connected with the destruction of blood cell structure.
Highlights
In biological systems, carbon monoxide (CO) is a gaseous second messenger and arises during the oxidative catabolism of heme by the heme oxygenase enzymes
Due to the lack of literature data concerning the influence of exogenous CO on the electrical properties of biological membranes, we examined changes in the surface charge of blood cells after fatal CO poisoning
The membrane surface charge density values in fatal CO poisoning presented here were compared with the membrane surface charge density values after sudden unexpected death obtained by us previously (Kotynska et al 2012)
Summary
Carbon monoxide (CO) is a gaseous second messenger and arises during the oxidative catabolism of heme by the heme oxygenase enzymes. Many biological functions of heme oxygenase, such as regulation of vessel tone, smooth muscle cell proliferation, neurotransmission, platelet aggregation and anti-inflammatory and antiapoptotic effects, have been attributed to its enzymatic product, CO (Bilban et al 2008). In physiological conditions heme oxygenases catabolize heme into three products: CO, biliverdin and free iron (Ryter et al 2006). Heme-derived CO has been proven to modulate neuronally mediated activities, acting as an important neuromodulator, and participates in the regulation of diverse cellular functions, including apoptosis of erythrocytes (Johnson and Johnson 2000). Sources of CO poisoning include motor vehicle exhaust fumes, poorly functioning heating systems and inhaled smoke (Satran et al 2005)
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