Disease relevance of Nonadecafluorodecanoic acid

• The objective of this study was to compare the effects of perfluorodecanoic acid (PFDA) and ciprofibrate on the induction of hepatic toxicity and on hepatocellular proliferation in rats [1].
• Cytotoxic and cytolytic activity of nonadecafluoro-n-decanoic acid on Acholeplasma laidlawii [2].
• Nonadecafluoro-n-decanoic acid (ND-FDA) has a single dose ip LD50 of 41 mg/kg and causes anorexia and a wasting syndrome [3].
• Treatment of L5178Y mouse lymphoma cells with perfluoro-n-decanoic acid (PFDA) in growth medium for 24 hr at 30 degrees C produces a dose-dependent inactivation of a channel in the cell membrane [4].
• PPAR alpha and ACO mRNA levels were increased rapidly in the rat hepatoma cell line FaO after treatment with PFDA or the prototypical peroxisome proliferator Wy 14,643 [5].

High impact information on Nonadecafluorodecanoic acid

• Effect of the peroxisome proliferators ciprofibrate and perfluorodecanoic acid on hepatic cell proliferation and toxicity in Sprague-Dawley rats [1].
• Effects of peroxisome proliferators on rat liver phospholipids: sphingomyelin degradation may be involved in hepatotoxic mechanism of perfluorodecanoic acid [6].
• Perfluorodecanoic acid (PFDA) reduced GSH S-transferase activity, prevented phorone-mediated GSH depletion and abolished either HO-1 or c-jun mRNA induction by phorone [7].
• Effect of the peroxisome proliferator perfluoro-n-decanoic acid on glucose transport in the isolated perfused rat liver [8].
• Perfluorodecanoic acid (PFDA) is a potent peroxisome proliferator and is known to affect hepatic lipid metabolism in rats [9].

Chemical compound and disease context of Nonadecafluorodecanoic acid

• Perfluoro-n-decanoic acid: induction of peroxisomal beta-oxidation by a fatty acid with dioxin-like toxicity [10].
• Despite demonstration of covalent binding of PFDA and PFOA to proteins both in vivo and in vitro, the role of this macromolecular binding in perfluorinated fatty acid toxicity is not known [11].
• We investigated the effect of the peroxisomal proliferator (PP) perfluorodecanoic acid (PFDA), alone or in combination with 9-cis-retinoic acid (RX) on the human glioblastoma cell line Lipari (LI) [12].

Biological context of Nonadecafluorodecanoic acid

• Effects of the peroxisome proliferator perfluoro-n-decanoic acid on hepatic gluconeogenesis and glycogenesis: a 13C NMR investigation [13].
• A sex difference in the fecal elimination of perfluorodecanoic acid (PFDA) was observed with 51 and 24% of the administered 14C being recovered in the feces of male and female rats, respectively, by 28 days post-treatment [14].
• Nuclear run-on experiments in vivo suggest that, unlike ACO, PFDA as well as caloric restriction results in accumulation of PPAR alpha mRNA which cannot be explained solely by transcriptional activation [5].
• Energy metabolism and body composition were investigated in perfluorodecanoic acid (PFDA)-treated rats (single i.p. dose of 20, 40 or 80 mg/kg) and their respective pair-fed counterparts 7 days after dosing [15].
• The effects of perfluorodecanoic acid (PFDA) on humoral, cellular, and innate immunity in Fischer 344 rats [16].

Anatomical context of Nonadecafluorodecanoic acid

• Both proteins are induced in rat liver by the potent peroxisome proliferator perfluorodecanoic acid (PFDA) [17].
• Effects of perfluorodecanoic acid on hepatic indices of thyroid status in the rat [18].
• At lethal concentrations, both PFOA and NDFDA possess detergent activity since they can release IgM in soluble form from a cell line that does not secrete immunoglobulins, and brief exposure (15 min) to 1-2 mM of both perfluorinated fatty acids results in solubilization of F4 cells equivalent to the anionic detergent deoxycholic acid [19].
• The toxicity of two perfluorinated fatty acids, penta decafluoro-n-octanoic acid (PFOA) and nonadecafluoro-n-decanoic acid (NDFDA), on three mammalian B cell lines was evaluated [19].
• The in vivo effects of perfluorodecanoic acid (PFDA) exposure on antibody production, delayed type hypersensitivity (DTH), and natural killer (NK) cell activity were determined [16].

Associations of Nonadecafluorodecanoic acid with other chemical compounds

• The purpose of this study was to determine if hepatic cellular antioxidants and indices of oxidative damage are altered by administration of the peroxisome proliferators ciprofibrate and perfluorodecanoic acid (PFDA) [20].
• Effects of perfluoro-n-octanoic acid, perfluoro-n-decanoic acid, and clofibrate on hepatic phosphorus metabolism in rats and guinea pigs in vivo [21].
• The histamine antagonist cimetidine and the peroxisome proliferator perfluorodecanoic acid are both potent inhibitors of f4A1 [22].
• A multiple regression analysis of the three parameters revealed that the data from rats treated with PFOA and PFDA shared one common line, indicating a marked correlation among the inductions of the three parameters [23].
• Peroxisome proliferator perfluorodecanoic acid alters glutathione and related enzymes [24].

Gene context of Nonadecafluorodecanoic acid

• The latter, alone or in association with PFDA, induces catalase activity and protein, increases apoptosis and decreases cell proliferation [12].
• Peroxisomal number and relative volume, as well as palmitoyl-CoA oxidase activity and protein, are increased by PFDA treatment, with a synergistic effect by RX [12].
• Modulation of selenium-dependent glutathione peroxidase by perfluorodecanoic acid in rats: effect of dietary selenium [25].
• Inhibition of long-chain acyl-CoA synthetase by the peroxisome proliferator perfluorodecanoic acid in rat hepatocytes [9].
• Messenger RNA levels for ACO increased rapidly in rat liver and declined over the subsequent 7 days following PFDA administration, while PPAR alpha mRNA increased slower and remained elevated over this period [5].

Analytical, diagnostic and therapeutic context of Nonadecafluorodecanoic acid

• Effects of perfluorodecanoic acid (PFDA, 20-80 mg/kg, ip) on the androgenic status of sexually mature male rats were investigated 7 days after treatment [26].
• Alterations in lipid metabolism were examined in adult male Sprague-Dawley rats seven days after a single intraperitoneal injection of perfluorodecanoic acid (PFDA; 20, 40 or 80 mg/kg) [27].
• In addition, PPAR alpha mRNA accumulation in PFDA-treated rats appears to be due primarily to hypophagia as pair feeding and complete caloric restriction result in a large increase in the concentration of this messenger RNA [5].
• The oral administration of powdered chow containing 0.02%-PFOA and PFBA to male rats of the Sprague-Dawley strain for 2 weeks and the single intraperitoneal injection of corn oil mixed with PFDA, PFOA, and PFOL at the dose of 100 mg/kg induced peroxisome proliferation markedly [28].
• Subtoxic concentrations of perfluorinated fatty acids (0.9 mM PFOA; 0.5 mM NDFDA) greatly diminish binding of MC540 by normal plasma membranes, as determined by fluorescence flow cytometry [29].

References