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Lead Toxicity in Chicks: Interactions With Dietary Methionine and Choline¹

Department of Poultry Science, North Carolina State University, Raleigh, NC 27695-7608

Two factorial experiments were conducted to study the effects of dietary methionine and choline on lead toxicity in chicks. Dietary variables were 0.3 or 0.63% (experiment 1) or 0.23 or 0.75% methionine (experiment 2); 0 or 1000 ppm lead (as Pb acetate · 3H₂O); and 1130 or 3300 mg/kg (experiment 1) or 396 or 1266 mg/kg choline (experiment 2). In both experiments, lead depressed growth while methionine stimulated growth. Growth depression by lead was less with methionine-adequate than with methionine-inadequate diets. There were no differences in growth with the choline-marginal or choline-excess diets. In experiment 2, the methionine x lead interaction for growth was observed with choline-adequate but not with choline-inadequate diets. Lead-induced depression of growth was exacerbated by added choline when methionine-inadequate diets were fed. With methionine-adequate diets, choline level had no effect on the lead-induced depression of growth. Hepatic nonprotein sulfhydryl (NPSH) concentrations were increased by both supplemental methionine and lead with no interaction. Choline levels had no effect on NPSH. Dietary methionine significantly lowered Pb concentration of kidney and muscle but not of bone, liver or blood. Choline had no effect on organ Pb concentrations. Methionine, either dietary or in the dosing solution, had no effect on in situ intestinal absorption or ²⁰³PbCl₂. The results suggest that lead lowers the chick's choline requirement and that the methyl moiety of methionine does not participate directly in lead detoxication. The amelioration of Pb toxicity by methionine appears to be related to increased excretion of Pb.

KEY WORDS: • Pb toxicity • choline • methionine • nutritional toxicology • growing chicks • organ lead concentration

¹ Paper No. 9536 of the Journal Series of the North Carolina Agricultural Research Service, Raleigh, NC 27695-7601.

² To whom reprint requests should be addressed.

Manuscript received 11 October 1985. Revision accepted 2 April 1986.