Atherogenic lipoproteins can cause endothelial dysfunction in the initial stage of atherogenesis. In our study we examined 134 patients with defined hyperlipoproteinemia (non-HDL cholesterol > 4.1 mmol/l or triglycerides > 2.5 mmol/l or taking any of lipid lowering drugs) – 94 men and 40 women. The subgroup of controls of comparable age contained 54 normolipidemic individuals – 30 men and 24 women. Patients with hyperlipoproteinemia revealed significantly lower ability of endothelium-dependent flow-mediated vasodilation (EDV) measured on brachial artery (4.13±3.07 vs. 5.41±3.82 %; p=0.032) and higher carotid intima media thickness than normolipidemic controls (0.68±0.22 vs. 0.58±0.15 mm; p=0.005). In regression analysis, EDV correlated significantly with plasma concentrations of oxLDL (p<0.05) HDL-cholesterol (p<0.05), Apo A1 (p<0.05), ATI (p<0.01) and non-HDL cholesterol (p<0.05). Patients with hyperlipoproteinemia showed higher plasma levels of oxLDL (65.77±9.54 vs. 56.49±7.80 U/l; p=0.015), malondialdehyde (0.89±0.09 vs. 0.73±0.08 µmol/l; p=0.010) and nitrites/nitrates (20.42±4.88 vs. 16.37±4.44 µmol/l; p=0.018) indicating possible higher long-term oxidative stress in these patients.
In this minireview, the factors involved in the development of corneal injury due to an increased amount of UVB rays are summarized. Experimental studies have shown that an increased number of UVB rays leads to a profound decrease in corneal antioxidants (high molecular weight, antioxidant enzymes as well as low molecular weight, mainly ascorbic acid) so that a prooxidant/antioxidant imbalance appears. The decrease of corneal antioxidant protective mechanisms results in oxidative injury of the cornea and causes damage of the inner parts of the eye by UVB rays and by reactive oxygen species generated by them.