Cellular Enrichment with Polyunsaturated Fatty Acids Induces an Oxidative Stress and Activates the Transcription Factors AP1 and NFκB

Mazière, Cécile; Conte, M; Degonville, James; Ali, Dany; Mazière, Jean‐Claude

doi:10.1006/bbrc.1999.1644

Cited by 149 publications

(86 citation statements)

References 34 publications

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“…These studies indicated that PHVF consumption renders the animals more vulnerable to inflammation as compared to those given oils containing cisunsaturated fatty acids. However, PUFA is also known to downregulates the production of inflammatory mediators like interleukins, CRP and metallo proteases (Mazière et al 1999). The n-3 PUFA can effectively decrease the arachidonic acid content in the membranes and limit its availability for the synthesis of pro inflammatory eicosanoids (Calder 2010).…”

Section: Discussionmentioning

confidence: 99%

“…The enzyme NADPH oxidase plays an important role in nonspecific host defense during infection by generating large quantities of superoxide anions. It has been demonstrated that vascular NADH/ NADPH oxidase significantly contributes to superoxide production, a mechanism through which PUFA is thought to enhance the antioxidant enzyme activities (Mazière et al 1999). Ojieh et al (2009) observed that the rats fed hydrogenated palm oil showed significantly reduced levels of GST, glutathione reductase, GPx activities compared to rats fed unhydrogenated palm oil.…”

Section: Discussionmentioning

confidence: 99%

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Diet containing partially hydrogenated vegetable fat enhances the carrageenan induced paw inflammation but not oxidative stress markers in liver of rats

Rao

Lokesh

2015

J Food Sci Technol

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In the present study, we investigated the effect of feeding Partially hydrogenated vegetable fat (PHVF) on carrageenan induced paw inflammation and oxidative stress markers in liver of rats. In addition, the effect of feeding rats with Linseed Oil (LSO, α-linolenic acid, n-3 PUFA) or PHVF blended with incremental amounts of LSO on these markers were also monitored. Rats weighing 200 g were given 1 mL of different oils (PHVF, Groundnut Oil; GNO, Olive Oil; OO and LSO) per day for 15 days. Rats given PHVF showed higher levels of paw inflammation in response to carrageenan injection. Rats given LSO showed least amounts of paw inflammation when injected with carrageenan. A second set of experiment was conducted by feeding weaning rats with AIN-93 purified diet supplemented with PHVF or PHVF with incremental amounts of LSO for 60 days. The rats fed PHVF showed higher degree of carrageenan induced inflammation as compared to rats given GNO and LSO. However, the rats fed PHVF showed lower levels of lipid peroxides, protein carbonyls, 8-hydroxy guanine and antioxidant enzyme activities in liver homogenate as compared to those given LSO. In conclusion dietary PHVF rendered the rats prone to higher levels of carrageenan induced inflammation which can be reduced by giving PHVF blended with LSO. However, oxidative stress markers found to be higher levels in rats given LSO or PHVF blended with LSO as compared to rats given PHVF as sole source of fat.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Diet containing partially hydrogenated vegetable fat enhances the carrageenan induced paw inflammation but not oxidative stress markers in liver of rats

Rao

Lokesh

2015

J Food Sci Technol

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“…Unlike LA, oleic acid did not induce peroxynitrite formation in endothelial cells. In contrast to other long-chain fatty acids, oleic acid is rather ineffective at inducing cellular oxidative stress (64). However, oleic acid has been reported to increase the production of NO in endothelial cells (65).…”

Section: Discussionmentioning

confidence: 99%

Linoleic acid-induced endothelial activation

Saraswathi

Toborek

et al. 2004

Journal of Lipid Research

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“…LPCs have been shown to induce demyelination (20,21) by activating cell death in mature oligodendrocytes and in oligodendrocyte progenitors (22,23). On the other hand, metabolism of AA gives rise to ROS, which induce oxidative stress, leading to either cell proliferation or apoptosis, depending on the cell type (24)(25)(26)(27) and also regulate redox-sensitive transcription factors AP-1 and NF-nB by activating p38 mitogen-activated protein kinase (MAPK) (28)(29)(30). Released free AA either acts as a second messenger or is further metabolized by three different enzyme systems, i.e.,cyclooxygenase, lipoxygenase, and cytochrome P450 epoxygenase, to generate eicosanoid signaling molecules, including prostaglandins, leukotrienes, and thromboxanes (31).…”

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confidence: 99%

Krabbe disease: psychosine-mediated activation of phospholipase A2 in oligodendrocyte cell death

Giri

Khan

Rattan

et al. 2006

Journal of Lipid Research

101

122

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Globoid cell leukodystrophy (Krabbe disease) is an inherited neurological disorder caused by the pathogenomic accumulation of psychosine (galactosylsphingosine), a substrate for the deficient enzyme galactocerebroside bgalactosidase. This study underscores the mechanism of action of psychosine in the regulation of oligodendrocyte cell death via the generation of lysophosphatidylcholine (LPC) and arachidonic acid (AA) by the activation of secretory phospholipase A2 (sPLA2). There was a significant increase in the level of LPC, indicating a phospholipase A2 (PLA2)-dependent pathobiology, in the brains of Krabbe disease patients and those of twitcher mice, an animal model of Krabbe disease. In vitro studies of the treatment of primary oligodendrocytes and the oligodendrocyte MO3.13 cell line with psychosine also showed the generation of LPC and the release of AA in a dose-and time-dependent manner, indicating psychosine-induced activation of PLA2. Studies with various pharmacological inhibitors of cytosolic phospholipase A2 and sPLA2 and psychosine-mediated induction of sPLA2 enzymatic activity in media supernatant suggest that psychosine-induced release of AA and generation of LPC is mainly contributed by sPLA2. An inhibitor of sPLA2, 7,7-dimethyl eicosadienoic acid, completely attenuated the psychosine-mediated accumulation of LPC levels, release of AA, and generation of reactive oxygen species, and blocked oligodendroyte cell death, as evident from cell survival, DNA fragmentation, and caspase 3 activity assays. This study documents for the first time that psychosine-induced cell death is mediated via the sPLA2 signaling pathway and that inhibitors of sPLA2 may hold a therapeutic potential for protection against oligodendrocyte cell death and resulting demyelination in Krabbe disease.-Giri, S

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Cellular Enrichment with Polyunsaturated Fatty Acids Induces an Oxidative Stress and Activates the Transcription Factors AP1 and NFκB

Cited by 149 publications

References 34 publications

Diet containing partially hydrogenated vegetable fat enhances the carrageenan induced paw inflammation but not oxidative stress markers in liver of rats

Diet containing partially hydrogenated vegetable fat enhances the carrageenan induced paw inflammation but not oxidative stress markers in liver of rats

Linoleic acid-induced endothelial activation

Krabbe disease: psychosine-mediated activation of phospholipase A2 in oligodendrocyte cell death

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