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Dietary Lead and Calcium: Effects on Blood Pressure and Renal Neoplasia in Wistar Rats^1,2,

John D. Bogden³, Sheldon B. Gertner^*, Francis W. Kemp, Robbie McLeod^*, Kay S. Bruening and Haingsub R. Chung

Departments of Preventive Medicine and Community Health ^* Pharmacology and Toxicology Pathology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, NJ 07103-2714

We examined the potential of increased Ca in the diet to modify the effects of Pb on tissue metal concentrations, blood pressure and the incidence of renal tumors. We randomly assigned 48, 5-wk-old male Wistar rats to one of six treatment groups. They were fed a low (0.2%) or high (4.0%) Ca diet for 31 wk and given 0, 1.0 or 100 µg Pb/mL in drinking water. In the low Ca groups, increasing concentrations of Pb produced graded increases in mean blood pressure. Rats receiving 4.0% Ca had higher mean blood pressures than the animals fed the 0.2% Ca diet. The 4.0% Ca diet also caused renal and urinary bladder stones to develop in some rats. The high Ca diet did not prevent dose-dependent increases in tissue Pb accumulation, but it caused significant decreases in kidney Cu, femur Mg and Fe in kidney, liver and testis. Femur Mg and Fe and liver Fe concentrations were lowest in rats receiving 4.0% Ca and 100 µg Pb/mL. Precancerous and cancerous renal lesions occurred to the greatest extent in the rats receiving 100 µg Pb/mL and the high Ca diet. These results suggest that high dietary Ca does not protect against Pb-induced increases in blood pressure or Pb accumulation in tissues and may often produce nephrocalcinosis. In addition, high dietary Ca in the presence of Pb may increase the incidence of renal tumors.

KEY WORDS: • lead • calcium • blood pressure • kidney tumors • rats

¹ Presented at the Meeting of the American Society for Pharmacology and Experimental Therapeutics, Salt Lake City, August 15, 1989, and at the UCLA Colloquium on the Inorganic Chemistry/Molecular Biology Interface, Taos, NM, February 28, 1990.

² Supported in part by the National Science Foundation Industry-University Cooperative for Research in Hazardous and Toxic Substances and the American Heart Association-New Jersey Affiliate.

³ To whom correspondence should be addressed.

Manuscript received 23 October 1989. Revision accepted 24 September 1990.

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