The effects of dietary calcium during lactation on lead in bone mobilization: implications for toxicology

Under a normal 1.0% calcium (Ca) concentration in the diet during and after chronic lead (Pb) intoxication, there was a significant increment in the concentration of Pb in the blood, kidney, liver and brain during lactation, parallel to a decrement of Pb in the bone. The increment of Pb in the brain was accompanied by an enhanced lipid oxidation (increase in conjugated dienes). During lactation, on the first 14 days, when dietary Ca was reduced to 0.05%, bone Ca concentration was decreased by 15%, bone resorption measured as acid phosphatase activity in plasma increased three times and Pb bone concentration dropped by 30%. Under a 0.05% Ca in the diet in the nonlactating rats, Ca in the bone decreases also, but there were neither increments in bone resorption nor Pb efflux from the bone. These results suggested that Pb efflux in the bone was related to bone resorption during lactation. Interestingly, when dietary Ca was enhanced to 2.5% in lactating rats, Ca concentration in the bone increased by 21%, but resorption did not decrease and Pb bone concentration decreased by 28%, enhancing toxicity. In the control Pb-exposed nonlactating rats under a 2.5% Ca in the diet, Ca concentration in the bone was increased (18%), and Pb concentration in the bone was unaltered. Since Ca metabolism changes drastically in humans during pregnancy and lactation, and it is likely that bone Pb is mobilized and transferred to the more available compartments of the maternal circulation, the increment in daily intake of Ca during lactation could enhance Pb efflux from the bone.