Transcription of genes involved in fat metabolism in chicken embryos exposed to the peroxisome proliferator-activated receptor alpha (PPAR伪) agonist GW7647 or to perfluorooctane sulfonate (PFOS) or perfluorooctanoic acid (PFOA)

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• 作者：Marie Strö ; mqvist^a ; ^{marie.stromqvist@ebc.uu.se} ; Jan A. Olsson^a ; Anna Kä ; rrman^b ; Bjö ; rn Brunströ ; m^a
• 关键词：PPAR ; PFOS ; PFOA ; Chicken ; Embryo
• 刊名：Comparative Biochemistry and Physiology ; Part C
• 出版年：2012
• 期刊代码：8_15320456
• 类别：pha
• 出版时间：June, 2012
• 卷：156
• 期：1
• 页码：29-36
• 文件大小：712 K

摘要

Perfluoroalkyl acids (PFAAs) such as perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are developmental toxicants in various animal classes, including birds. Both compounds interact with peroxisome proliferator-activated receptors (PPARs), but it is not known whether activation of PPARs is involved in their embryo toxicity in birds. We exposed chicken embryos via egg injection at a late developmental stage to GW7647, a potent PPAR伪 agonist in mammals, and to PFOS or PFOA. Mortality was induced by PFOS and PFOA but not by GW7647. Transcripts of a number of genes activated by PPAR伪 agonists in mammals were analyzed in liver and kidney of 18-day-old embryos. Several of the genes were induced in both liver and kidney following exposure to GW7647. Treatment with PFOA resulted in induction of acyl-coenzyme A oxidase mRNA in liver, whereas none of the genes were significantly induced by PFOS treatment. No up-regulation of gene transcription was found in kidney following treatment with PFOS or PFOA. Principal component analysis showed that PFOA caused an mRNA expression pattern in liver more similar to the pattern induced by GW7647 than PFOS did. Our findings do not support that the embryo mortality by PFOS and PFOA in chicken embryos involves PPAR伪 activation.