Gene expression profiling in the liver and lung of perfluorooctane sulfonate-exposed mouse fetuses: comparison to changes induced by exposure to perfluorooctanoic acid.
Perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) are environmental contaminants found in the tissues of humans and wildlife. They are activators of peroxisome proliferator-activated receptor-alpha (PPAR alpha) and exhibit hepatocarcinogenic potential in rats. PFOS and PFOA are also developmental toxicants in rodents and PFOS has been shown to induce pulmonary deficits in rat offspring. Pregnant CD-1 mice were dosed with 0, 5, or 10mg/kg PFOS from gestation days 1-17. Transcript profiling was conducted on the fetal liver and lung. Results were contrasted to data derived from a previous PFOA study. PFOS-dependent changes were primarily related to activation of PPAR alpha. No remarkable differences were found between PFOS and PFOA. Given that PPAR alpha signaling is required for neonatal mortality in PFOA-treated mice but not those exposed to PFOS, the neonatal mortality observed for PFOS may reflect functional deficits related to the physical properties of the chemical rather than to transcript alterations.
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA. Electronic address: rosen.mitch@epa.gov.
Mitchell B
MB
Rosen
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
Judith E
JE
Schmid
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
Kaberi P
KP
Das
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
Carmen R
CR
Wood
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
Robert D
RD
Zehr
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Reproductive Toxicology Division, Research Triangle Park, NC, USA.
Christopher
C
Lau
D017738:Alkanesulfonic Acids / Q000494:pharmacology / Q000633:toxicity*; D000818:Animals; D002210:Caprylates / Q000494:pharmacology / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005333:Fetus / Q000378:metabolism; D005466:Fluorocarbons / Q000494:pharmacology / Q000633:toxicity*; D020869:Gene Expression Profiling; D008099:Liver / Q000378:metabolism*; D008168:Lung / Q000378:metabolism*; D018811:Maternal Exposure; D051379:Mice; D008815:Mice, Inbred Strains; D046228:Microarray Analysis; D011247:Pregnancy
D017738:Alkanesulfonic Acids; D002210:Caprylates; D005466:Fluorocarbons; C023036:perfluorooctanoic acid; C076994:perfluorooctane sulfonic acid