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Lead mobilization during calcium disodium ethylenediaminetetraacetate chelation therapy in treatment of chronic lead poisoning.

It has long been established that chronic lead (Pb) poisoning is a cause of renal insufficiency. However, although easily diagnosed, there is still no treatment available that will revert this type of poisoning. We report a study performed on 56 male Wistar rats administered Pb in drinking water (500 ppm Pb acetate) over a 90-day period. Twenty-one non-Pb-exposed animals served as the control group. Seven animals from each group were killed days 60 and 90. At the end of the 90-day period, 21 of the Pb-exposed animals were treated with disodium monocalcium EDTA (50 mg/kg/d for 5 days) intraperitoneally and 21 animals were administered serum saline by the same route. Three treatment courses were administered, separated by 9 days free of treatment. Seven animals from each subgroup were killed at the end of each treatment course. Pb levels were determined in blood, urine, liver, brain, kidney, and bone. Treatment with EDTA led to a greater and more rapid reduction in Pb contents in the brain and kidney. The decrease in hepatic Pb levels in the treated group of animals was similar to that in the group administered placebo. Bone Pb levels also failed to show a response to the chelating agent. Use of EDTA appears to result in a reduction in Pb deposits in such critical organs as the kidney and brain. However, the chelating agent does not seem to have access to bone Pb deposits, such that the skeleton becomes a permanent source of poisoning for other tissues.

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