Erythrocyte membrane dysfunctions

Several in vitro studies proved that treatment of intact erythrocytes with nitrites causes the oxidation of hemoglobin to methemoglobin by radical generation along with a decrease in reduced glutathione (GSH) level associated with erythrocyte membrane dysfunctions and namely altered cell ionic flux, lipid peroxidation, and perturbation of membrane transport (Batina et al 1990 May et al 2000). Nitrate/ nitrite-induced oxidation of biological molecules potentiates reactions, which interfere in the oxidative chain and which can affect some antioxidant systems. 

Moreover, we very recently reported that erythrocyte membrane AChE activity in MTHFR C677T carriers was found significantly higher when Hey levels in their blood were increased. In contrast, the erythrocyte manbrane enzyme activity was restored nearly to normal when the individual Hey levels decreased. The AChE activation observed may be implicated in cholinergic mechanisms (e.g., vasodilatation, neurological dysfunction) through modulatiou of acetylcholine production (Schulpis et al., 2005). 

Observational studies In a comparison of HBOC-201 and erythrocyte transfusion, the former caused mild platelet dysfunction, which may be caused by reactive oxygen molecules. In blood, there is redox hemostasis as a result of a trans-plasma membrane redox system in platelets. This hemostasis could be impaired by free radicals [23 ]. 

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