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Dietary Calcium Modifies Concentrations of Lead and Other Metals and Renal Calbindin in Rats1,2,

John D. Bogden, Sheldon B. Gertner*, Sylvia Christakos{dagger}, Francis W. Kemp, Zhengang Yang, Suzanne R. Katz and Ching Chu{dagger}

Departments of Preventive Medicine and Community Health * Pharmacology and Toxicology {dagger} Biochemistry and Molecular Biology, University of Medicine and Dentistry of New Jersey—New Jersey Medical School, Newark, NJ 07103-2714

We studied the effects of dietary calcium on kidney, femur, testis, liver, heart and brain concentrations of lead, magnesium, iron, copper, calcium and zinc in rats exposed to lead for 1 y. Renal levels of the 28,000 Da, vitamin D-dependent, calcium-binding protein calbindin-D28K were also measured. Seventy-two weanling male Sprague-Dawley rats were randomly assigned to one of nine treatment groups. Rats were fed diets containing 0.1, 0.5 or 2.5% Ca for 52 wk and were simultaneously given either 0, 50 or 100 mg lead/L in their drinking water. Rats fed the 0.1% Ca diet had organ lead concentrations that were two- to 20-fold greater than the corresponding animals fed 0.5% Ca. Rats fed diets containing 2.5% Ca had the lowest organ lead concentrations. Despite substantial effects of diet Ca on organ lead concentrations, Ca did not significantly influence concentrations of most other divalent metals studied with the exception of kidney calcium and magnesium, testis iron, plasma ionic calcium and magnesium, and several femur metals. Kidney calcium concentrations were lower in rats fed 2.5% Ca diets than in those fed 0.1 or 0.5% Ca diets. For rats not given lead, renal calbindin concentrations were highest in rats fed 0.1% Ca, and lowest in rats fed 2.5% Ca. Lead inhibited an increase in renal calbindin in the rats fed 0.1% Ca, but paradoxically increased renal calbindin levels in animals fed 2.5% Ca.


KEY WORDS: • calcium • lead • calbindin • rats

1 Presented in part at the meeting: Nutrition and the Central Nervous System, Lake Tahoe, CA, February 3, 1992.

2 Supported in part by a grant from the American Heart Association—New Jersey Affiliate.

Manuscript received 16 October 1991. Revision accepted 6 February 1992.




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