Physiological importance of ω-3/ω-6 polyunsaturated fatty acids in man. An overview of still unresolved and controversial questions

Debry, G; Pelletier, Xavier

doi:10.1007/bf01945421

Cited by 23 publications

(5 citation statements)

References 69 publications

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“…The amplified toxicity of linoleic acid and PCBs to endothelial cells could thus be mediated by cellular accumulation of this fatty acid and its subsequent transformation to toxic cytotoxic epoxide metabolites (Viswanathan et al 2003). Because of the very low basal activity of endothelial cell delta-6 desaturase, arachidonic acid is not produced from linoleic acid significantly in this type of cell (Debry and Pelletier 1991; Spector et al 1981), which can result in linoleic acid accumulation within endothelial cells (Hennig and Watkins 1989; Spector et al 1981). Furthermore, Matsusue et al (1999) demonstrated that coplanar PCBs can suppress delta-5 and delta-6 desaturase activities.…”

Section: Discussionmentioning

confidence: 99%

Dietary Fat Interacts with PCBs to Induce Changes in Lipid Metabolism in Mice Deficient in Low-Density Lipoprotein Receptor

Hennig¹,

Reiterer²,

Toborek³

et al. 2005

Environ Health Perspect

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There is evidence that dietary fat can modify the cytotoxicity of polychlorinated biphenyls (PCBs) and that coplanar PCBs can induce inflammatory processes critical in the pathology of vascular diseases. To test the hypothesis that the interaction of PCBs with dietary fat is dependent on the type of fat, low-density lipoprotein receptor–deficient (LDL-R−/−) mice were fed diets enriched with either olive oil or corn oil for 4 weeks. Half of the animals from each group were injected with PCB-77. Vascular cell adhesion molecule-1 (VCAM-1) expression in aortic arches was non-detectable in the olive-oil–fed mice but was highly expressed in the presence of PCB-77. PCB treatment increased liver neutral lipids and decreased serum fatty acid levels only in mice fed the corn-oil–enriched diet. PCB treatment increased mRNA expression of genes involved in inflammation, apoptosis, and oxidative stress in all mice. Upon PCB treatment, mice in both olive- and corn-oil–diet groups showed induction of genes involved in fatty acid degradation but with up-regulation of different key enzymes. Genes involved in fatty acid synthesis were reduced only upon PCB treatment in corn-oil–fed mice, whereas lipid transport/export genes were altered in olive-oil–fed mice. These data suggest that dietary fat can modify changes in lipid metabolism induced by PCBs in serum and tissues. These findings have implications for understanding the interactions of nutrients with environmental contaminants on the pathology of inflammatory diseases such as atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Dietary Fat Interacts with PCBs to Induce Changes in Lipid Metabolism in Mice Deficient in Low-Density Lipoprotein Receptor

Hennig¹,

Reiterer²,

Toborek³

et al. 2005

Environ Health Perspect

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show abstract

“…The amplified toxicity of linoleic acid and PCBs to endothelial cells could also be mediated by cellular accumulation of this fatty acid and thus its availability as a substrate for the formation of cytotoxic epoxide metabolites. Due to the very low basal activity of endothelial cell delta 6-desaturase, arachidonic acid is not produced from linoleic acid significantly in this type of cell (Spector et al, 1981;Debry and Pelletier, 1991), which can result in linoleic acid accumulation within endothelial cells (Spector et al, 1981;Hennig and Watkins, 1989). Furthermore, Matsusue et al (1999) demonstrated that coplanar PCBs can suppress delta 5 and delta 6 desaturase activities.…”

Section: Discussionmentioning

confidence: 99%

The Role of Methyl-Linoleic Acid Epoxide and Diol Metabolites in the Amplified Toxicity of Linoleic Acid and Polychlorinated Biphenyls to Vascular Endothelial Cells

Slim

Hammock

Toborek

et al. 2001

Toxicology and Applied Pharmacology

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“…Prolonged diet supplementation with polyunsaturated fatty acids (PUFA) has been shown to induce signi®cant changes in membrane lipid composition both in animals (Biagi et al 1991;Kinsella 1990) and in humans (Debry and Pelletier 1991;Guezennec et al 1989;Levin et al 1992) and to lead to an increase in membranē uidity (Levin et al 1992;Stubbs et al 1981) and red blood cell deformability (Guezennec et al 1989;Tsuda and Masuyama 1990). In the light of the potential inuence of these observations on oxygen transfer across the alveolocapillary membrane, we have examined, in a previous study, the eects of PUFA administration on the extent of exercise-induced hypoxaemia.…”

Section: Introductionmentioning

confidence: 96%

Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxaemia in master athletes

Aguilaniu¹,

Flore²,

Page³

et al. 1997

European Journal of Applied Physiology

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We have previously reported a reduction in exercise-induced hypoxaemia following polyunsaturated fatty acid supplementation (PUFA). Although this might have been explained by increases in membrane fluidity, a clear explanation could not be provided due to potentially confounding influences of series-2 prosta- glandin mediated effects resulting from PUFA. In this investigation, ten master athletes [mean age 48.1 (SEM 6) years, maximal oxygen uptake (VO2max) 3.39 (SEM 0.21) l x min(-1)] completed a maximal cycling test (Ctrl) which was repeated after the administration of 150 mg of indomethacin to inhibit prostaglandin synthesis, both before and after 6 weeks of 3.66-g PUFA x day(-1). Cardiorespiratory parameters were obtained simultaneously with brachial arterial blood sampling for partial pressure of oxygen in arterial blood (PaO2), partial pressure of carbon dioxide in arterial blood (PaCO2), pH, oxygen saturation in arterial blood and lactate concentration determinations. A significant decrease in PaO2 (mmHg) from rest [93 (SEM 1.5)] was observed for exercise intensities of more than 40% VO2max in Ctrl reaching 75.9 (SEM 2.1) at VO2max. PUFA resulted in a 5.0 (SEM 0.68) mmHg upward shift (P < 0.05) in the PaO2-oxygen uptake relationship, reducing the difference in partial pressure of oxygen between alveolar air and arterial blood (P(A-a)O2) at VO2max [Ctrl 36 (SEM 1.6) vs PUFA 33 (SEM 2.2) mmHg] while PaCO2, remained unchanged. Indomethacin had no effect on either PaO2, ideal partial pressure of oxygen in alveolar gas or P(A-a)O2 in either Ctrl or after PUFA. In contrast, the fall in pH was significantly reduced after indomethacin while VCO2, PaCO2 and lactacidaemia remained unchanged. These observations confirm an effect of PUFA on exercise PaO2 behaviour which does not appear to be mediated by the influence of a series-2 prostaglandin.

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Physiological importance of ω-3/ω-6 polyunsaturated fatty acids in man. An overview of still unresolved and controversial questions

Cited by 23 publications

References 69 publications

Dietary Fat Interacts with PCBs to Induce Changes in Lipid Metabolism in Mice Deficient in Low-Density Lipoprotein Receptor

Dietary Fat Interacts with PCBs to Induce Changes in Lipid Metabolism in Mice Deficient in Low-Density Lipoprotein Receptor

The Role of Methyl-Linoleic Acid Epoxide and Diol Metabolites in the Amplified Toxicity of Linoleic Acid and Polychlorinated Biphenyls to Vascular Endothelial Cells

Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxaemia in master athletes

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