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Lead-exposure of neonatal rats through maternal milk : A confounded model
A A Mylroie1, C Tucker, L Rosselli-Austin
1Department of Physical Sciences, Chicago State University, 60628, Chicago, IL.
Insights
Maternal feces significantly increase lead (Pb) exposure in neonatal rat pups. Coprophagy (fecal consumption) by pups, combined with high Pb levels in dam feces, elevates Pb concentrations in pups
Area of Science:
- Toxicology
- Developmental Biology
- Animal Models
Background:
- Neonatal rats exposed to lead (Pb) serve as a model for childhood plumbism.
- Pups are typically assumed to ingest Pb solely through maternal milk.
- Rat pups exhibit coprophagy, consuming maternal feces starting in the second postnatal week.
Purpose of the Study:
- To investigate if maternal feces are a significant source of Pb exposure in pups nursed by a Pb-exposed dam.
- To quantify the impact of fecal Pb ingestion on pup Pb levels.
Main Methods:
- Dams received lead acetate (PbAc) via drinking water (500 ppm) or intubation (3 mg/kg) from P1 to P21.
- Pups had controlled access to maternal feces (Pb-containing or Pb-free) during lactation.
- Pb concentrations were measured in pup blood, brain, bone, and liver at P21.
Main Results:
- Feces from Pb-exposed dams contained 1000–5000 μg Pb/g wet weight.
- Pups with access to contaminated feces showed 2-4 times higher Pb concentrations in blood, brain, bone, and liver.
- This effect was observed even when Pb exposure was primarily via maternal milk.
Conclusions:
- Maternal feces represent a substantial Pb exposure route for neonatal rat pups.
- Coprophagy and high fecal Pb content are critical factors in pup Pb exposure.
- These factors must be considered when modeling lead toxicity in young animals.
Abstract:
Lead-exposed neonatal rats are frequently used as a model for plumbism in children. In most studies,PPb is administered to the dam, and it is assumed that the pups are exposed to Pb primarily from the dam's milk. Rat pups, however, are coprophagic and begin to consume the maternal feces in their second postnatal week. This experiment was designed to determine whether the maternal feces are a significant source of Pb in pups exposed via the lactating dam. Dams were administered Pb as lead acetate (PbAc), either through their drinking water (500 ppm PbAc) or through twice daily intubations (3 mg PbAc/Kg body wt) from postpartum d 1 (P1) to P21 (P0=day of birth). Control dams were administered deionized water. The dams were housed with their litters in stainless-steel hanging cages with wire-screened bottoms. Litters of exposed and control dams treated through their drinking water had access to either Pb-containing or Pb-free maternal fecal matter for 2 h/d during the late lactation period. Half of the litters from intubated dams had continuous access to maternal feces throughout the lactation period, whereas access was curtailed at P14 in the other litters. Lead content of the feces from Pb-exposed dams ranged from 1000 to 5000 μg Pb/g wet wt. At P21, Pb concentrations were 2-4 times higher in blood, brain, bone, and liver of pups that had access to Pb-contaminated feces than in pups that were exposed to Pb primarily through the mother's milk. When estimating exposure levels in pups receiving Pb through the lactating dam, coprophagy and the high content of Pb in the dam's feces must be taken into consideration.
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