OBJECTIVE: Exposure to lead (Pb) has been shown to disrupt many processes in cells, including disorders in the metabolism of high energy nucleotides (ATP, GTP). In erythrocytes, a normal level of nucleotides is necessary for these cells to fulfill their basic physiological functions. The reactions of the phosphoribosyltransferases: adenine APRT (EC 2.4.2.7) and hypoxanthine-guanine HGPRT (EC 2.4.2.8) enable the salvage of purine bases (adenine, guanine and hypoxanthine), converting them to nucleotides (AMP, GMP, IMP respectively), and as purines cannot be synthesized de novo, they are the main source of mononucleotides for the synthesis of high energy nucleotides. The aim of this paper is to evaluate the influence of chronic exposure to lead ions on the parameters of energy status and the activity of the erythrocyte APRT and HGPRT in rats.

MATERIALS AND METHODS: The study was performed on 20 sexually mature, 3-month old male Wistar rats, which were given ad libitum 1% of lead acetate (PbAc) for 9 months. The concentrations of purines (ATP, ADP, AMP, Ado, GTP, GDP, GMP, Guo) in whole blood were determined with HPLC. The activity of HGPRT and APRT was measured by examining the increase in IMP and AMP, respectively, for 20 min of the hemolysate incubation in the presence of PRPP, with hypoxanthine and adenine as substrates. Their activities were converted into mg of Hb in hemolysate and expressed in nmol/mg Hb/min. Pb concentration in whole blood was determined by AAS.

RESULTS: Lead-treated animals had a significantly higher concentration of lead in their blood (6.98 ± 1.43 mg/dL compared to the control group 0.32 ± 0.65 mg/dL (p<0.05). We observed a significant lead-induced decrease in whole blood ATP concentration (by 32 %, p<0.05) and AEC value (by 8%, p<0.05) together with an increase in ADP (28.5%, p<0.05), AMP (27%, p<0.0 5) and Ado (by 56%, p<0.05). In the control groups the mean activities of APRT and HGPRT were respectively: 0.745±0.067 and 3.580±0.115 nmol/mg Hb/min. In the groups of rats intoxicated by lead we observed a decrease in APRT by ca. 35 %, and a decrease in HGPRT by 30% vs the control (p< 0.033 for both).

CONCLUSION: The exposure to lead impairs red blood cell energy metabolism, and in consequence the functioning of the erythrocytes. The shorter life of the erythrocytes, their earlier hemolysis and higher susceptibility to oxidative stress, all observed in the exposure to lead, may result from the impairment of the erythrocyte energy metabolism, due to the decrease in the activity of salvage pathway enzymes.

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