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Remy R (Inst. Physiol. Vet. Coll.). Experimental studies on lead poisoning in animals. I. Toxicology. II. Therapy and prophylaxis. Deutsche Tierurztliche Wochenschrift. 1956; 63:385-388; 405-408 (Oct. 1; 15). (692) [Pb poisoning in man and animals is briefly reviewed with special emphasis on hematological findings in acute and chronic intoxication. In a study of acute Pb poisoning in 2-3 kg rabbits, Pb acetate was given iv on 3 successive days at levels of 2, 4, 6, 7, and 8 mg/kg, respectively. The 7 and 8 mg/kg dose levels of Pb acetate were uniformly lethal and death occurred before there was pronounced anemia. Anemia occurred at other dosage levels, but was followed by recovery. It was noted further that pure strain rabbits (Blue Vienna and Angora) died at a Pb dosage of 5 mg/kg. Very fat rabbits and growing rabbits also showed a lower tolerance to Pb acetate. A series of experiments was also carried out on a large number of 150-g rats, employing ip injection of Pb acetate after it was found that such injections did not cause local inflammation. Rats receiving Pb acetate at 150 mg/kg in 1 injection died within 24 hr; of those receiving Pb acetate at 50 mg/kg, none died. In the last group a repeat dose after several days produced no deaths, but further injections to a total of 200 mg of Pb produced death regularly. In another group of rats give Pb acetate injections of 15 mg/kg at regular intervals for 2 mo, practically all animals were alive after reaching a total dosage of 360 mg. Further, these subacutely poisoned rats now uniformly withstood a 100 mg/kg dose of Pb acetate with no deaths, and 4 days later they again tolerated a further 100 mg/kg but 40% of them died within 10 days. The remainder outlived the research period and thus tolerated total Pb acetate dosage of 560 mg/kg.
These findings are discussed with reference to hemoglobin and nucleoprotein synthesis and hemopoiesis, and the interference of Pb in these systems is postulated as being mediated through folic-folinic acid and vitamin B12-containing enzymes.
II. Large doses of Vitamin B12, folic acid, or liver extract helped retard or prevent the appearance of anemia in animals acute poisoned with Pb, but had no beneficial effect in chronic Pb poisoning. Cysteine, given iv, was beneficial in acute Pb poisoning but not in subacute poisoning; cystine was ineffective in either case. Oral methionine (30-40 mg/kg) effectively retarded or prevented the onset of anemia, but was ineffective n reducing skeletal deposition of Pb. BAL was completely ineffective. For animals poisoned acutely with Pb, a complete protein hydrolyzate plus vitamin B12 injection gave better protection against anemia than either material alone. Oral or injected methionine alone was also inferior to the mixture in its protection against anemia. Ascorbic acid was an equally effective preventive of Pb-induced anemia of dogs but was ineffective in rats for acute and subacute poisoning. As to CaNa2EDTA treatment, 33 rats were poisoned by ip injections of Pb acetate, 35 mg/kg, every 4 days to a total of 315 mg. At the same time, EDTA was given by esophageal tube to 17 of these animals 6 times/wk in doses of 294 mg/kg to a total of 7938 mg/kg. The remaining 16 rats served as controls: 80% died and the remainder showed severe poisoning symptoms. All the EDTA-treated rats lived, and seemed well. For the controls, the reticulocyte curves were from 2-3 times normal, but the treated rats had essentially normal curves. This may indicate prevention of bone-marrow damage. It is concluded that the EDTA is effective prophylactically against Pb poisoning as well as for acute, subacute, and chronic Pb poisoning. Oral EDTA and methionine are suggested for chronic Pb poisoning.

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