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  • Early postnatal lead exposure induces tau phosphorylation in the brain of young rats.

Early postnatal lead exposure induces tau phosphorylation in the brain of young rats.

Acta biologica Hungarica (2012-11-09)
A Rahman, K M Khan, G Al-Khaledi, I Khan, Sreeja Attur
ABSTRACT

Cognitive impairment is a common feature of both lead exposure and hyperphosphorylation of tau. We, therefore, investigated whether lead exposure would induce tau hyperphosphorylation. Wistar rat pups were exposed to 0.2% lead acetate via their dams' drinking water from postnatal day 1 to 21. Lead in blood and brain were measured by atomic absorption spectrophotometry and the expression of tau, phosphorylated tau and various serine/threonine protein phosphatases (PP1, PP2A, PP2B and PP5) in the brain was analyzed by Western blot. Lead exposure significantly impaired learning and resulted in a significant reduction in the expression of tau but increased the phosphorylation of tau at Ser199/202, Thr212/Ser214 and Thr231. PP2A expression decreased, whereas, PP1 and PP5 expression increased in lead-exposed rats. These results demonstrate that early postnatal exposure to lead decrease PP2A expression and induce tau hyperphosphorylation at several serine and threonine residues. Hyperphosphorylation of tau may be a mechanism of Pb-induced deficits in learning and memory.

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%