Differential expression of chicken hepatic genes responsive to PFOA and PFOS.
The effects of PFOS and PFOA on the gene expression patterns of chickens that were exposed to either PFOS or PFOA at low doses were investigated with the use of microarray techniques. Twelve Genechip Chicken Genome Arrays were used to study hepatic gene expression in 6-week-old chickens (Gallus gallus) that were exposed to either PFOA (0.1, 0.5, or 5mg/mL), PFOS (0.02 or 0.1mg/mL), or a saline vehicle control (0.9% NaCl in Milli-Q water) via subcutaneous implantation of a 2mL osmotic pump for 4 weeks or for 4 weeks with a further 4 weeks of depuration. Over 240 and 480 genes were significantly affected by PFOS after 4 weeks of exposure and after 4 weeks of exposure with a further 4 weeks of depuration, respectively and over 290 and 320 genes were significantly affected by PFOA, correspondingly. For PFOS, the genes that were affected after 4 weeks of exposure were mainly related to the transport of electrons and oxygen, and the metabolism of lipids and fatty acids; while the genes that were affected after 4 weeks of exposure with a further 4 weeks of depuration were mainly related to the transport of electrons and ions, and protein amino acid phosphorylation and proteolysis. For PFOA, the genes that were affected after 4 weeks of exposure were related to the transport of ions, lipids, and electrons and cytochromes; while the genes that were affected after 4 weeks of exposure with a further 4 weeks of depuration were related to protein amino acid phosphorylation and proteolysis, the transport of ions, and the metabolism of fatty acids and lipids. The results also showed that the gene expression patterns between chickens that were treated with PFOS and those that were treated with PFOA were different, which points to the importance of the separate evaluation of the toxicities of PFOS and PFOA. Specifically, the gene expressions of CYP8B and NOV were studied.
Yeung
Leo W Y
LWY
Safety Research Team, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki 305-0856, Japan; Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon, Hong Kong, China.
Guruge
Keerthi S
KS
Safety Research Team, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki 305-0856, Japan. Electronic address: guruge@affrc.go.jp.
Yamanaka
Noriko
N
Safety Research Team, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki 305-0856, Japan.
Miyazaki
Shigeru
S
Safety Research Team, National Institute of Animal Health, Kannondai 3-1-5, Tsukuba, Ibaraki 305-0856, Japan.
Lam
Paul K S
PKS
Department of Biology and Chemistry, City University of Hong Kong, Tat Chee Avenue, Kowloon, Hong Kong, China. Electronic address: bhpksl@cityu.edu.hk.
D017738:Alkanesulfonic Acids / Q000633:toxicity*; D000818:Animals; D002210:Caprylates / Q000633:toxicity*; D002645:Chickens / Q000235:genetics / Q000254:growth & development / Q000378:metabolism; D015536:Down-Regulation; D005466:Fluorocarbons / Q000633:toxicity*; D015870:Gene Expression / Q000187:drug effects*; D020869:Gene Expression Profiling; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D015854:Up-Regulation
D017738:Alkanesulfonic Acids; D002210:Caprylates; D005466:Fluorocarbons; C023036:perfluorooctanoic acid; C076994:perfluorooctane sulfonic acid