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Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development
1Department of Physiology, University of Western Australia, Perth.
Insights
Iron deficiency increases lead absorption but does not elevate brain lead levels in rats. Lead intoxication does not affect iron uptake in the brain or kidneys, though it can increase liver iron stores.
Area of Science:
- Toxicology
- Nutritional Science
- Neuroscience
Background:
- Environmental lead intoxication and iron deficiency are common pediatric health issues.
- Iron deficiency can enhance intestinal lead absorption, suggesting a metabolic interaction.
- Understanding this interaction is crucial for assessing lead's neurotoxic potential in children.
Purpose of the Study:
- To investigate the interplay between iron deficiency and lead exposure on tissue lead and iron levels.
- To determine the impact of iron status on lead and iron uptake in the brain and other organs.
- To evaluate the role of the blood-brain barrier in regulating lead accumulation.
Main Methods:
- Rats of varying ages (15, 21, 63 days) were subjected to different dietary lead and iron conditions.
- Tissue lead and nonheme iron concentrations were measured.
- Iron-59 (59Fe) uptake was assessed after intravenous injection of transferrin-bound 59Fe.
Main Results:
- Iron deficiency increased intestinal lead absorption, evidenced by higher blood and kidney lead levels.
- Brain lead levels remained low (<0.1 microgram/g) and were not increased by iron deficiency.
- Iron deficiency enhanced 59Fe uptake in the brain, while lead intoxication did not affect iron uptake in the brain or kidneys.
Conclusions:
- The blood-brain barrier significantly limits lead entry into the brain, irrespective of iron status.
- Lead intoxication at the levels studied did not impair iron uptake in the brain or kidneys.
- Iron deficiency, not lead, is the primary driver of increased iron uptake in the brain.
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.