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Microglial disruption in young mice with early chronic lead exposure.

Toxicology letters (2013-04-20)
Christina Sobin, Mayra Gisel Flores Montoya, Natali Parisi, Tanner Schaub, Miguel Cervantes, Rodrigo X Armijos
ABSTRACT

The mechanisms by which early chronic lead (Pb) exposure alter brain development have not been identified. We examined neuroimmune system effects in C57BL/6J mice with Pb exposure, including levels that may be common among children in lower socioeconomic income environments. Pups were exposed via dams' drinking water from birth to post-natal day 28 to low, high or no Pb conditions. We compared gene expression of neuroinflammatory markers (study 1); and microglial mean cell body volume and mean cell body number in dentate gyrus, and dentate gyrus volume (study 2). Blood Pb levels in exposed animals at sacrifice (post-natal day 28) ranged from 2.66 to 20.31μg/dL. Only interleukin-6 (IL6) differed between groups and reductions were dose-dependent. Microglia cell body number also differed between groups and reductions were dose-dependent. As compared with controls, microglia cell body volume was greater but highly variable in only low-dose animals; dentate gyri volumes in low- and high-dose animals were reduced. The results did not support a model of increased neuroinflammation. Instead, early chronic exposure to Pb disrupted microglia via damage to, loss of, or lack of proliferation of microglia in the developing brains of Pb-exposed animals.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Lead(II) acetate trihydrate, ≥99.99% trace metals basis
Sigma-Aldrich
Lead(II) acetate trihydrate, 99.999% trace metals basis
Sigma-Aldrich
Lead(II) acetate trihydrate, JIS special grade, ≥99.5%
Sigma-Aldrich
Lead(II) acetate trihydrate, ACS reagent, ≥99%
Sigma-Aldrich
Lead(II) acetate trihydrate, puriss. p.a., ACS reagent, reag. ISO, reag. Ph. Eur., 99.5-102.0%