Ciprofibrate treatment in patients with atherogenic lipoprotein phenotype:effects on HDL quality, LDL susceptibility to oxidation and DNA damage

Objectives: This study was conducted to examine a complex effect of ciprofi brate therapy in patients with atherogenic lipoprotein phenotype. Methods: Effects of ciprofibrate were studied on HDL subpopulations, HDL ab ility to esterify cholesterol (FERHDL), susceptibility of LDL to oxidation as well as on in vivo oxidative DNA damage in peripheral lymphocytes, measu red as strand breaks (SBs) by the comet assay. Results: Ciprofibrate treatment significantly decreased total cholesterol, and triglycerides, and increased HDL-cholesterol. The FERHDL showed a signi ficant reduction (29.5 +/-; 7.4 to 23 +/- 7.5% . h(-1), P = 0.0001). The re lative concentrations of HDL subclasses did not differ between baseline and after treatment. Ciprofibrate induced a significant increase in LDL oxidat ion lag time (93 +/- 7 to 102 +/- Ii min, P = 0.02) and a decrease in DNA s trand breaks (34.0 +/- 16.2 to 17.8 +/- 7.5, P = 0.02). A significant corre lation between maximal rate of diene production and strand breaks was found (r = 0.55, P = 0.01). These findings may be explained by an improvement of LDL resistance to oxidation, resulting in a decrease in oxidatively modifi ed LDL's cytotoxic effect. Conclusion: Ciprofibrate treatment favourably affected the quality of plasm a HDL, probably by the improvement of triglyceride rich lipoprotein metabol ism and/or LDL subpopulation profile, increased LDL resistance to oxidation , and decreased the level of DNA damage in peripheral lymphocytes.