Polychlorinated biphenyls (PCBs)
are persistent organic pollutants (POPs), which accumulates in the food chain
due to their lipophilicity, bioaccumulation and biomagnification properties.
Despite the industrial production of PCBs being banned since late 1980s because
of their negative impact on the human body and environment, high concentrations
of PCBs still can be detected on air, food, water and human samples.
Although recent epidemiological
studies have reported a body of evidences suggesting that chronic PCB exposure
has contributed to a rising risk of metabolic disorders, especially obesity and
type 2 diabetes mellitus (T2DM), the underlying
mechanisms involved in the metabolic side-effects of PCB exposure are still
not clear.Studies carried on by our group over the last years have revealed
important aspects regarding the effects of PCB126 intoxication on metabolic
function.The PCB126 is considered the most toxic among PCBs congeners and its
biological effects are mediated by binding and activation of the cytoplasmic
aryl hydrocarbon receptor (AhR), inducing the transcription and expression of
AhR target genes.
Recently, our group has reported
that long-term intranasal exposure to low doses of PCB126 impaired G protein
coupled receptor (GPCR) signalling in circulating leukocytes and impaired
innate immunological functions related to the host's defence to infections on
rats. Intriguingly, PCB126 exposure resulted in PC126 accumulation on liver and
up-regulated AhR expression on liver and visceral adipose tissue, which are
tissues that are important for regulating the glucose and lipid metabolism.
No comments:
Post a Comment