Dose-related effects of perfluorodecanoic acid on growth, feed intake and hepatic peroxisomal β-oxidation

Borges, Tim; Robertson, Larry W.; Peterson, Richard E.; Glauert, Howard P.

doi:10.1007/bf02307265

Cited by 32 publications

(10 citation statements)

References 28 publications

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“…The liver is the target organ of accumulation for PFOS (Borges et al 1978;Butenhoff and Seacat 2001;Pastoor et al 1987). The concentration of PFOS in the liver was 2-3-fold greater than that found in serum.…”

Section: Discussionmentioning

confidence: 98%

“…PFOS has been detected in the liver and blood plasma of wildlife on a global scale (Giesy and Kannan 2001). Exposure to PFOS affects the liver primarily and causes vacuolation and hypertrophy of hepatic cells (Borges et al 1978; Butenhoff and Seacat 2001;Pastoor et al 1987). PFOS also decreases body weight (BW), serum cholesterol, and triglycerides and increases liver weight (Butenhoff and Seacat 2001;Seacat et al 2002).…”

mentioning

confidence: 98%

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Neuroendocrine effects of perfluorooctane sulfonate in rats.

Austin

Kasturi

Barber

et al. 2003

Environ Health Perspect

295

173

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Perfluorooctane sulfonate (PFOS) is a degradation product of sulfonyl-based fluorochemicals that are used extensively in industrial and household applications. Humans and wildlife are exposed to this class of compounds from several sources. Toxicity tests in rodents have raised concerns about potential developmental, reproductive, and systemic effects of PFOS. However, the effect of PFOS on the neuroendocrine system has not been investigated thus far. In this study, adult female rats were injected intraperitoneally with 0, 1, or 10 mg PFOS/kg body weight (BW) for 2 weeks. Food and water intake, BW, and estrous cycles were monitored daily. At the end of treatment, PFOS levels in tissues were measured by high-performance liquid chromatography (HPLC) interfaced with electrospray mass spectrometry. Changes in brain monoamines were measured by HPLC with electrochemical detection, and serum corticosterone and leptin were monitored using radioimmunoassay. Treatment with PFOS produced a dose-dependent accumulation of this chemical in various body tissues, including the brain. PFOS exposure decreased food intake and BW in a dose-dependent manner. Treatment with PFOS affected estrous cyclicity and increased serum corticosterone levels while decreasing serum leptin concentrations. PFOS treatment also increased norepinephrine concentrations in the paraventricular nucleus of the hypothalamus. These results indicate that exposure to PFOS can affect the neuroendocrine system in rats.

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Section: Discussionmentioning

confidence: 98%

mentioning

confidence: 98%

Neuroendocrine effects of perfluorooctane sulfonate in rats.

Austin

Kasturi

Barber

et al. 2003

Environ Health Perspect

295

173

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“…The increased level of C ") : " in the livers of rats following the administration of a single high dose of PFDA has been suggested to be caused by mobilization from peripheral stores [8,9] and by the inhibition of peroxisomal β-oxidation [30]. In the present study, however, a linear correlation was confirmed between the proportion of C ") : " in microsomal lipid and the activity of ∆*desaturase in microsomes isolated from the livers of rats in five different physiological states (control, starved, starved\refed, clofibric acid-fed and PFDA-fed).…”

Section: Discussionmentioning

confidence: 99%

Perfluorodecanoic acid enhances the formation of oleic acid in rat liver

Yamamoto

Kawashima

1997

Biochemical Journal

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The feeding of perfluorodecanoic acid (PFDA) to male rats at a dietary concentration of 0.005% (w/w) for 7 days resulted in a marked increase in the activity of microsomal stearoyl-CoA desaturation in the liver. This increase in the overall desaturation activity was due to the induction of terminal desaturase among the components comprising the desaturation system. In contrast, PFDA inhibited desaturation in vitro, seemingly due to interference with electron transport through the desaturation system. Accordingly, PFDA can be an inducer and also an inhibitor of delta9-desaturation. PFDA feeding enhanced the conversion of radioactive stearic acid into oleic acid in the liver in vivo, indicating that the induction of delta9-desaturase by PFDA functions in vivo. PFDA feeding increased the mass of octadecenoic acid (C18:1) in the liver and the proportion of C18:1 in microsomal lipid. A highly significant linear correlation existed between the microsomal desaturase activity and the proportion of C18:1 in microsomal lipid when compared using rats in five different physiological states: control, PFDA-fed, p-chlorophenoxyisobutyric acid (clofibric acid)-fed, starved and starved/refed. These results suggest that the increase in the hepatic level of C18:1 caused by feeding of PFDA to rats can be explained by the common concept of regulation, i.e. the hepatic level of C18:1 is under the control of delta9-desaturase. The dietary administration of PFDA also increased the content of cytochrome P-450 and the activity of 7-ethoxycoumarin O-de-ethylase in the liver.

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“…Additionally, GSH and GSSG can be eliminated from liver by the action of transpeptidases and via bile secretion [13,31]. Contrast to many peroxisome proliferators, PFDA treatment lowers the flux through peroxisomal b-oxidation, even though it induced peroxisomal FAO activity as other peroxisome proliferators [32,33]. PFDA inhibits several enzymes involved in peroxisomal b-oxidation, which may decrease the rate of peroxisomal b-oxidation and H 2 0 2 production [34], but it had no effect on GSHPX [14].…”

Section: Figurementioning

confidence: 94%

Peroxisome proliferator perfluorodecanoic acid alters glutathione and related enzymes

Chen

Tatum

Glauert

et al. 2001

J Biochem & Molecular Tox

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Previously we have shown that treatment with the peroxisome proliferator perfluorodecanoic acid (PFDA) significantly increased hepatic reduced glutathione (GSH) content without altering the activity of selenium-glutathione peroxidase. In this study we examined some potential mechanisms by which PFDA treatment increases GSH levels. Male Sprague-Dawley rats were given a single injection of 0, 8.8, 17.5, and 35 mg PFDA in corn oil per kg body weight. Twelve days later the effects of PFDA on the activities of enzymes associated with GSH synthesis, utilization, and regeneration were assessed. The results showed that in a dose-dependent manner, PFDA treatment significantly decreased the activity of gamma-glutamylcysteine synthetase, while the activities of NADPH-generating enzymes, malic enzyme, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase were increased. PFDA treatment also dose dependently decreased cytosolic, but not microsomal, glutathione S-transferase activity, and the activity of glutathione reductase was decreased by the highest dose of PFDA. The data obtained suggest that increased hepatic GSH levels following PFDA treatment may result from increased regeneration and/or decreased utilization.

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Dose-related effects of perfluorodecanoic acid on growth, feed intake and hepatic peroxisomal β-oxidation

Cited by 32 publications

References 28 publications

Neuroendocrine effects of perfluorooctane sulfonate in rats.

Neuroendocrine effects of perfluorooctane sulfonate in rats.

Perfluorodecanoic acid enhances the formation of oleic acid in rat liver

Peroxisome proliferator perfluorodecanoic acid alters glutathione and related enzymes

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