Effect of the increased level of Lead on in-vitro serum lipid peroxidation

Background: Lead is a heavy metal that enters the human body through the environmental pollution such as air. Lead contamination is associated with the increased cardiovascular diseases, but the exact mechanism is not fully clarified. The aim of this study was to evaluate the effect of Lead on lipid peroxidation. Materials and Methods: In this in vitro experimental study, a pool serum was prepared from the healthy subjects and divided into the five fractions. With the addition of Lead, its concentrations in the four samples reached to 0.5, 1, 4 and 5 μM and the fifth sample was used as control. Samples were incubated at 37 °C for one day. Lipid oxidation was induced in each diluted sample by the addition of Cu2+. Oxidation profile was monitored by reading of OD at 245nm. A number of quantitative parameters including the lag-time, maximal rate of oxidation (V-max), and maximal amount of lipid peroxide products (OD-max) were evaluated. Results: The lag-times in the Lead samples were 4 and 5 µM (158±1.7) and (149.3±1.3) decreased compared to the control (169.7±0.5). Moreover, OD-max in the samples (0.399±0.003) and (0.409±0.008) increased compared to the control (0.373±0.01, P<0.05). Conclusion: The results show that Lead in high concentrations can trigger serum lipid oxidation. Since the experimental concentrations were in the borderline of toxicity to humans, Lead contamination may increase the risk of cardiovascular disease by enhanced lipid peroxidation

The effect of Mercury on in-vitro serum lipid oxidizability

Background: Mercury is a toxic metal which participate in the environmental pollution. Toxic dose of mercury cause various diseases such as cardiovascular and mental with not fully understood mechanism. The aim of this study was to evaluate the effect of Mercury in serum lipid oxidizability. Material and Methods: In this in vitro experimental study, serum pools of healthy subjects were prepared and divided into six fractions. Mercury concentration in five fractions increased to 20, 30, 50, 200, 700 nM and the sixth fraction was considered as a control. Samples were incubated at 37° C for 24 hours and serum lipid oxidation was followed by monitoring of the absorbance change at 245nm in diluted serum after the addition of Cu2+. A number of quantitative parameters including lag-time, maximal rate of oxidation (V-max), and maximal amount of lipid peroxide products (OD-max) were evaluated. Results: Lag-time in all concentrations of the experiment 20, 30, 50, 200, 700 nM were (18.7±.95), (18.5±0.57), (18.5±0.57), (24.2±2.9) and (14.7±2.7), respectively which decreased compared to the control (33±2.4) and V-max in 700nM (43.7±1.2) increased compared to the control (40±1.15, P<0.05). Conclusion: Results show that Mercury in all experimental concentrations whether tolerable or toxic causes accelerating serum lipid oxidation. According to its transmission special attention should be given to this metal