Abstract
Lead (Pb)-induced hypertension is characterized by an increase in reactive oxygen species (ROS) and a decrease in nitric oxide (NO). In the present study we evaluated the effect of L-arginine (NO precursor), dimercaptosuccinic acid (DMSA, a chelating agent and ROS scavenger), and the association of L-arginine/DMSA on tissue Pb mobilization and blood pressure levels in plumbism. Tissue Pb levels and blood pressure evolution were evaluated in rats exposed to: 1) Pb (750 ppm, in drinking water, for 70 days), 2) Pb plus water for 30 more days, 3) Pb plus DMSA (50 mg kg(-1) day(-1), p.o.), L-arginine (0.6%, in drinking water), and the combination of L-arginine/DMSA for 30 more days, and 4) their respective matching controls. Pb exposure increased Pb levels in the blood, liver, femur, kidney and aorta. Pb levels in tissues decreased after cessation of Pb administration, except in the aorta. These levels did not reach those observed in nonintoxicated rats. All treatments mobilized Pb from the kidney, femur and liver. Pb mobilization from the aorta was only effective with the L-arginine/DMSA treatment. Blood Pb concentrations in Pb-treated groups were not different from those of the Pb/water group. Pb increased blood pressure starting from the 5th week. L-arginine and DMSA treatments (4th week) and the combination of L-arginine/DMSA (3rd and 4th weeks) decreased blood pressure levels of intoxicated rats. These levels did not reach those of nonintoxicated rats. Treatment with L-arginine/DMSA was more effective than the isolated treatments in mobilizing Pb from tissues and in reducing the blood pressure of intoxicated rats.
Highlights
The levels of Pb in blood, kidney, femur, liver and aorta, as well as the evolution of blood pressure were evaluated in: 1) rats exposed to Pb (750 ppm, in the form of Pb acetate in their drinking water ad libitum) for 70 days (Pb group), and rats that received water or sodium acetate during the same period, 2) rats exposed to Pb for 70 days and receiving water for 30 additional days (Pb/water group), and rats that received water for 100 days, and 3) rats exposed or not to Pb that later received dimercaptosuccinic acid (DMSA) (25 mg/kg, orally by gastric gavage, twice a day for 6 days per week), L-arginine (0.6% in their drinking water ad libitum), and the combination of L-arginine/ DMSA for 30 additional days
The data demonstrated that all treatments were effective in mobilizing Pb from the kidney, femur and liver, except for the DMSA treatment, which did not mobilize Pb from the femur (Table 1)
Pb mobilization from the aorta was only effective with the L-arginine/DMSA treatment (Table 1)
Summary
The levels of Pb in blood, kidney, femur, liver and aorta, as well as the evolution of blood pressure were evaluated in: 1) rats exposed to Pb (750 ppm, in the form of Pb acetate in their drinking water ad libitum) for 70 days (Pb group), and rats that received water (water group) or sodium acetate (supplying an identical amount of acetate) during the same period, 2) rats exposed to Pb for 70 days and receiving water for 30 additional days (Pb/water group), and rats that received water for 100 days (water group), and 3) rats exposed or not to Pb that later received DMSA (25 mg/kg, orally by gastric gavage, twice a day for 6 days per week) (water/DMSA or Pb/DMSA groups), L-arginine (0.6% in their drinking water ad libitum) (water/L-arginine or Pb/L-arginine groups), and the combination of L-arginine/ DMSA (water/L-arginine/DMSA or Pb/Larginine/DMSA groups) for 30 additional days. Pb exposure caused an increase in the levels of this metal in the blood, liver, femur, kidney and aorta (Table 1). These levels did not reach the values observed in rats not exposed to Pb (Table 1).
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