AI Article Synopsis

  • Dioxin-like (DL) compounds are environmental pollutants that alter gene expression by binding to the aryl hydrocarbon receptor (AhR), leading to gene activation via a specific DNA mechanism.
  • * This research focused on how these compounds affect gene expression in bovine blood lymphocytes, as cattle are a significant source of human exposure through meat and dairy.
  • * The study found that DL compounds significantly increased the levels of certain genes (like CYP1A1 and CYP1B1) and identified factors that could inhibit this gene induction, suggesting the need for more research on these effects in live animals.

Article Abstract

The exposure to dioxin-like (DL) compounds, an important class of persistent environmental pollutants, results in the altered expression of target genes. This occurs through the binding to the aryl hydrocarbon receptor (AhR), the subsequent dimerization with the AhR nuclear translocator (ARNT), and the binding of the complex to DNA responsive elements. A number of genes are up-regulated, including, among others, the AhR repressor (AHRR) and several biotransformation enzymes, such as the members of CYP1 family and NAD(P)H-quinone oxidoreductase (NOQ1). The expression and the inducibility of the above genes were investigated in mitogen-stimulated cultured blood lymphocytes from cattle, which represent a notable source of DL-compound human exposure through dairy products and meat. As assessed by real-time PCR, all the examined genes except CYP1A2 and NQO1 were detected under basal conditions. Cell exposure to the DL-compounds PCB126 or PCB77 in the 10(-6)-10(-9)M concentration range resulted in a 2-4-fold induction of CYPIA1 and CYP1B1, which was antagonized by α-naphthoflavone or PCB153. This study demonstrates for the first time the presence and inducibility of the AhR pathway in easily accessible cells like bovine peripheral lymphocytes and prompts further investigations to verify whether similar changes could occur under in vivo conditions.

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Source
http://dx.doi.org/10.1016/j.toxlet.2011.07.014DOI Listing

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