The level of cytokines and features of inflammation in rat brain after oral exposure to polychlorinated biphenyls and brominated flame retardants | Health & Environmental Research Online (HERO)

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Citation
Tags

HERO ID

2158845

Reference Type

Journal Article

Subtype

Abstract

Title

The level of cytokines and features of inflammation in rat brain after oral exposure to polychlorinated biphenyls and brominated flame retardants

Author(s)

Dabrowska-Bouta, B; Frontczak-Baniewicz, M; Sulejczak, D; Sulkowski, G; Lenkiewicz, A; Struzynska, L

Year

2011

Is Peer Reviewed?

Journal

Pharmacological Reports
ISSN: 1734-1140
EISSN: 2299-5684

Volume

Issue

Page Numbers

1288

Language

English

DOI

10.1016/S1734-1140(11)70676-4

Web of Science Id

WOS:000298779300052

Abstract

Epidemiological studies have demonstrated that human exposure to polychlorinated biphenyls (PCBs) and brominated flame retardants (BFRs) during development causes long-lasting changes in nervous system functioning, and these findings are supported by experimental studies in several animal models. Tetrabromobisphenol-A (TBBPA) is a main representative of a large group of brominated flame retardants (BFRs), which are additives to plastics, textiles and electronic equipment to reduce their combustibility. Aroclor 1254, one of the PCBs, has been extensively used and dispersed from industrial applications worldwide and it is ubiquitous in the environment. Our study was designed to assess the effects of developmental exposure to PCBs and BFRs on the profile of cytokines in immature rats brain. Aroclor 1254 and TBBP-A were administered to the rats by oral gavage for two weeks. Exposure to Aroclor 1254 induced inflammatory response in rats, significantly elevating proinflammatory cytokines IL-6 (25%), IL-1beta (50%) and TNF-alpha (45%) over control values. We also observed increase in the level of these cytokines in rats exposed to TBBP-A (IL-6 – 60%; IL-1beta – 30% and TNF-alpha – 30%). These changes were associated with microglial activation. Light and electron-microscopic studies revealed morphological features in microglial cells connected with the activated state which were characteristic for both groups of exposed animals. Obtained results indicate that activation of microglia with coexisting inflammation is a common mechanism of PCBs and BFRs neurotoxicity in immature rat brain.

Conference Name

Neurochemical Conference 2011

Conference Location

Warsaw, Poland

Conference Dates

October 20-21, 2011