Effects of perfluoro-n-octanoic acid, perfluoro-n-decanoic acid, and clofibrate on hepatic phosphorus metabolism in rats and guinea pigs in vivo

• Published in: Toxicology and applied pharmacology Vol. 124; no. 2; p. 165
• Main Authors: Reo, N V, Goecke, C M, Narayanan, L, Jarnot, B M
• Format: Journal Article
• Language: English
• Published: United States 01-02-1994
• Subjects: Animals; Caprylates - pharmacology; Clofibrate - pharmacology; Decanoic Acids - pharmacology; Dose-Response Relationship, Drug; Fluorocarbons - pharmacology; Guinea Pigs; Injections, Intraperitoneal; Liver - drug effects; Liver - metabolism; Male; Phosphorus - metabolism; Rats; Rats, Inbred F344; Species Specificity
• ISSN: 0041-008X
• DOI: 10.1006/taap.1994.1020

Phosphorus-31 nuclear magnetic resonance (NMR) spectroscopy was used to study the effects of perfluoro-n-octanoic acid (PFOA), perfluoro-n-decanoic acid (PFDA), and clofibrate (CLOF) on liver phosphorus metabolism in rats and guinea pigs in vivo. All three compounds are known to cause peroxisome proliferation in rats but not in guinea pigs. The data indicate that indices related to overall tissue viability (i.e., adenosine triphosphate levels) remain unaffected at the doses and experimental times investigated for all treatments and both species. PFDA-treated rats revealed a marked increase in a liver phosphomonoester resonance compared with corresponding controls (p < or = 0.01); no such effect was observed in guinea pigs. This particular 31P NMR signal was identified as phosphocholine (PCho) and was found to steadily increase in concentration at consecutive days post-PFDA treatment, reaching 6.26 +/- 0.29 mumol/g liver at 5 days. This is fourfold greater than the PCho levels determined in livers from corresponding pair-fed control rats. The elevation in liver PCho is a specific response of PFDA treatment in rats and is not simply related to peroxisome proliferation in general, since neither PFOA nor CLOF produce such an effect. The data suggest a unique effect of PFDA on liver phospholipid metabolism, specifically phosphatidylcholine, which may involve enhanced phospholipid turnover via phosphatidylcholine-specific phospholipase C activity.