Decrease in the bioavailability of vasoactive nitric oxide (NO), derived from the
endothelial nitric oxide synthase (NOS3), underlines vascular endothelial damage.
Our expanding knowledge on mature red blood cells (RBCs) makes it supposable that
RBCs might contribute to vascular function and integrity via their active NO synthetizing
system (RBC-NOS3). This "rescue" mechanism of RBCs could be especially important during
pregnancy with smoking habit, when smoking acts as an additional stressor and causes
active change in the redox status. In this study RBC populations of 82 non-smoking
(RBC-NS) and 75 smoking (RBC-S) pregnant women were examined. Morphological variants
were followed by confocal microscopy and quantified by a microscopy based intelligent
analysis software. Fluorescence activated cell sorting was used to examine the translational
and posttranslational regulation of RBC-NOS, Arginase-1 and the formation of the major
product of lipid peroxidation, 4-hydroxy-2-nonenal. To survey the rheological parameters
of RBCs like elasticity and plasticity atomic force microscopy-based measurement was
applied. Significant morphological and functional differences of RBCs were found between
the non-smoking and smoking groups. The phenotypic variations in RBC-S population,
even the characteristic biconcave disc-shaped cells, could be connected to impaired
NOS3 activation and are compromised in their physiological properties. Membrane lipid
studies reveal an elevated lipid oxidation state well paralleled with the changed
elastic and plastic activities. These features can form a basic tool in the prenatal
health screening conditions; hence the compensatory mechanism of RBC-S population
completely fails to sense and rescue the acute oxidative stress conditions.
