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Indexed by:期刊论文

Date of Publication:2016-03-10

Journal:TOXICOLOGY

Included Journals:SCIE、PubMed、Scopus

Volume:347

Page Number:40-46

ISSN No.:0300-483X

Key Words:PFOS; Tau phosphorylation; Amyloid protein; Alzheimer's disease; Learning and memory

Abstract:With regard to the defects of the cognitive function observed after developmental exposure to perfluorooctane sulfonate (PFOS), and earlier studies on the developmental neurotoxicology, the aim of this study was to investigate the role of developmental PFOS exposure in neurodegenerative disorders in later life. Two pathological hallmarks of Alzheimer's disease (AD), Tau hyperphosphorylation and beta-amyloid (A beta) aggregation, were examined. SD rats were exposed to PFOS during only prenatal and/or postnatal period. Tau mRNA and protein levels were elevated by PFOS exposure. The phosphorylation of Tau at S199, T231 and S396 sites were also increased. Besides, PFOS exposure increased the A beta 1-42 levels, as well as the amyloid precursor protein (APP) regulation. The prenatal PFOS exposure caused alterations in the involved proteins at comparable levels with the postnatal and both prenatal and postnatal exposure. Thus, it has raised some evidence that early PFOS exposure can affect processes linked to neurodegeneration, enhancing the AD pathological risk. And PFOS exposures in early life may be of particular etiologic importance of neurodegenerative diseases. (C) 2016 Elsevier Ireland Ltd. All rights reserved.