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Perfluoro‐n‐decanoic acid: Induction of peroxisomal β‐oxidation by a fatty acid with dioxin‐like toxicity
Author(s) -
Harrison Earl H.,
Lane J. Scott,
Luking Scott,
Van Rafelghem Marc J.,
Andersen Melvin E.
Publication year - 1988
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02535290
Subject(s) - peroxisome , endoplasmic reticulum , biochemistry , mitochondrial toxicity , catalase , chemistry , fatty acid , oxidase test , toxicity , cytochrome c oxidase , mitochondrion , enzyme , organic chemistry , gene
Perfluoro‐n‐decanoic acid (PFDA) produces toxic effects in rodents similar to those caused by 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin. A single, intraperitoneal dose (50 mg/kg) of PFDA to Sprague‐Dawley rats caused disruption of the endoplasmic reticulum, mitochondrial swelling and increases in intracellular lipid droplets in hepatocytes similar to effects reported previously in dioxin toxicity. PFDA treatment led to large decreases in the activity of plasma membrane alkaline phosphodiesterase and mitochondrial cytochrome c oxidase without affecting lysosomal N‐acetyl‐β‐glucoaminidase, endoplasmic reticulum NADPH‐cytochrome c reductase or peroxisomal catalase activities. PFDA treatment led to moderate peroxisome proliferation and to very large (20–40‐fold) increases in the activity of fatty acyl‐CoA oxidase, the rate‐limiting enzyme in the peroxisomal system of fatty acid β‐oxidation.