Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development

Abstract

Environmental lead intoxication, which frequently causes neurological disturbances, and iron deficiency are clinical problems commonly found in children. Also, iron deficiency has been shown to augment lead absorption from the intestine. Hence, there is evidence for an interaction between lead and iron metabolism which could produce changes in lead and iron uptake by the brain and other tissues. These possibilities were investigated using 15-, 21-, and 63-old rats with varying nutritional iron and lead status. Dams were fed diets containing 0 or 3% lead-acetate and 0.2% lead-acetate in the drinking water. After weaning, 0.2% lead-acetate in the drinking water became the sole source of dietary lead. Measurements were made of tissue lead and nonheme iron levels and the uptake of 59Fe after intravenous injection of transferrin-bound 59Fe. Iron deficiency was associated with increased intestinal absorption of lead as indicated by blood and kidney lead levels in rats exposed to dietary lead. However, iron deficiency did not increase lead deposition in the brain, and in all rats brain lead levels were relatively low (< 0.1 microgram/g). Lead concentrations in the liver were below 2 micrograms/g, whereas kidneys had almost 20 times this concentration. Animals with iron deficiency had lower liver iron levels and had increased brain 59Fe uptake in comparison to control rats. However, iron levels in brain and kidneys were unaffected by lead intoxication regardless of the animal's iron status. 59Fe uptake rates were also unaffected by lead, but increased rates of uptake were apparent in iron-deficient rats. Lead did increase liver iron levels in all iron-adequate rats, but iron deficiency had little effect. It is concluded that, compared with other tissues, the blood-brain barrier largely restricts lead uptake by the brain and that the uptake that does occur is unrelated to the iron status of the animal. Also, the level of lead intoxication produced in this investigation did not influence iron uptake by the brain and kidneys, but liver iron stores could be increased if iron levels were already adequate.

Maternal blood lead concentration, diet during pregnancy, and anthropometry predict neonatal blood lead in a socioeconomically disadvantaged population.

“…Because heavier women are unlikely to gain as much weight and arm circumference as smaller ones, gain becomes an especially Our analysis of maternal diet provides new information on nutrient-lead interactions because it pertains to the transfer of lead from mother to fetus whereas most published research examines relationships of dietary intake and lead levels in either adults or children. In the APILS sample, higher maternal intakes of iron are associated with lower neonatal lead levels, a finding consistent with results from both experimental animal studies (Barton et al 1978;Crowe and Morgan 1996;Hamilton 1978;Hashmi et al 1989aHashmi et al , 1989bKlauder and Petering 1975;Mahaffey-Six and Goyer 1972;Ragan 1977;Shukla et al 1990;Singh et al 1991;Suzuki and Yoshida 1979) and human studies (Cheng et al 1998;Hammad et al 1996;Mahaffey and Annest 1986;Markowitz et al 1990;Szold 1974;Watson et al 1980Watson et al , 1986Wright et al 1999;Yip et al 1981;Yip and Dallman 1984) that have shown negative associations between iron intake or iron status and blood lead levels. Despite this negative relationship between maternal dietary iron and infant lead levels, we found no significant association between mother's iron stores (serum ferritin) and newborn's blood lead levels in bivariate or multivariate analysis (data not shown), mirroring the results of Milman and colleagues (1988).…”

Ingestion of Mn and Pb by rats during and after pregnancy alters iron metabolism and behavior in offspring

“…Offspring of iron-replete dams exposed to 3% Pb acetate in food and 0.2% in drinking water were intravenously injected with Tf-bound 59 Fe. The results showed no effects on brain and kidney iron uptake and enhanced uptake in the liver (Crowe and Morgan, 1996). …”

Mechanisms of divalent metal toxicity in affective disorders

“…Pb, along with other divalent metals, can be transported by DMT1 [222,223]. Iron deficiency in both animals and humans results in increased blood Pb levels [224,225]. Moreover, Wang et al [212,226] demonstrated that iron supplementation reduces both blood and brain Pb levels in the rats exposed to Pb and therefore provides a protective role against Pb-induced brain toxicity.…”