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The lipid profile (total cholesterol, HDL-cholesterol and triglycerides) was not affected either by cadmium treatment or by monensin therapy. The study by Messner et al. (2009) demonstrated that the plaque formation induced by Cd did not always correlate with alteration of the lipid profile. The authors concluded that Cd exerted its atherogenic activity by causing endothelial damage (Messner et al., 2009). Figure 5 Lipid profile in serum of the experimental animals. Each column represents mean��SD, n=6; Asterisk (*) represents significant differences between the Cd-treated group and normal controls, pLX4211 supplier significantly improved the morphology of both organs studied (data not shown). The data from the atomic absorption analysis showed that the highest Cd concentrations were measured in the kidneys and hearts of the Cd-treated animals (second group) (Figures 6 and ?and7).7). The values for the concentration of Cd in both organs are higher than those reported in our previous study where the animals were subjected to 10 mg/kg Cd(II) acetate daily treatment for 2 weeks (Ivanova et al., 2012). The data presented in this study confirmed that accumulation of Cd in the organs was dose dependent. Monensin decreased the Cd concentration in the kidneys and heart of Cd-intoxicated animals by 57 and 64%, respectively (p RG-6016 purchase the conclusion that the polyether ionophorous antibiotic monensin could be a promising ALK chelating agent for the treatment of renal dysfunction and cardiac impairment in cases of Cd intoxication. Figure 6 Cd concentration in kidneys of the experimental animals. Each column represents mean��SD, n=6; Asterisk (*) represents significant differences between the Cd-treated group and normal controls (p