Protective effects of dietary EPA and DHA on ischemia–reperfusion-induced intestinal stress

Brahmbhatt, Viral; Oliveira, Armando M.; Briand, Muriel; Perrisseau, Geneviève; Schmid, Viktoria Bastic; Destaillats, Frédéric; Pace-Asciak, Cecil R.; Benyacoub, Jalil; Bosco, Nabil

doi:10.1016/j.jnutbio.2012.02.014

Cited by 34 publications

(37 citation statements)

References 48 publications

(54 reference statements)

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“…Therefore, this research evidenced that in addition to an adequate dietary proportion between ω-6 and ω-3 PUFA, the proportion between marine ω-3 type lipids is also important and its intake could contribute towards the prevention of chronic inflammation and oxidative stress processes that have been correlated with metabolic syndrome, CVD, obesity, diabetes or even cancer [2,3]. Previous studies also supported the evidence of the protective effect of EPA and DHA intakes [16,31]. …”

Section: Resultssupporting

confidence: 64%

“…In detail, ARA ω-6 eicosanoids like PGE 2 and 11HETE, have been widely studied and identified as a key pro-inflammatory signaling molecules related with pro-aggregating, vasoconstrictive and immunosuppressive processes [9]; and they have also been associated with promotion of different human cancers including colon, lung, breast, head or neck [3]. On the other hand, derived eicosanoid and docosanoids from EPA and DHA have been related with protective effects on inflammation diseases [16], the regulation of tumor factors [18], or the reduction of CVD risk [10]. However, hydroxides and hydroperoxides derived from EPA and DHA were also considered as biomarkers of oxidative stress and weaker inflammatory substances than the corresponding ARA derivates [2,31].…”

Section: Discussionmentioning

confidence: 99%

“…The reduction of the intestinal injury was associated with the decline of oxidative stress, the up-regulation of 8isoPGF 3α (anti-inflammatory marker derived from EPA), and down-regulation of ARA pro-inflammatory metabolites (i.e. PGE 2 , LTB 4 , PGD 2 , Trioxilin A 3 and B 3 ) [16]. In a similar way, McDaniel et al have suggested that EPA:DHA (1.3:1) supplements may alter inflammation indexes in human plasma and blister fluids.…”

Section: Introductionmentioning

confidence: 99%

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Healthy effect of different proportions of marine ω-3 PUFAs EPA and DHA supplementation in Wistar rats: Lipidomic biomarkers of oxidative stress and inflammation

Dasilva

Pazos

García-Egido

et al. 2015

The Journal of Nutritional Biochemistry

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Dietary intervention with ω-3 marine fatty acids may potentially modulate inflammation and oxidative stress markers related with CVD, metabolic syndrome and cancer. The aim of this study was to evaluate whether different proportions of ω-3 EPA and DHA intake provoke a modulation of the production of lipid mediators and then, an influence on different indexes of inflammation and oxidative stress in a controlled dietary animal experiment using Wistar rats. For such scope, a lipidomic SPE-LC-ESI-MS/MS approach previously developed was applied to determine lipid mediators profile in plasma samples. The effect of ω-3 fatty acids associated to different ratios EPA:DHA was compared with the effect exerted by ω-3 ALA supplementation from linseed oil and ω-6 LA from soybean oil. CRP showed a tendency to greater inflammatory status in all ω-3-fed animals. Interestingly, ratios 1:1 and 2:1 EPA:DHA evidenced a noteworthy healthy effect generating a less oxidative environment and modulating LOX and COX activities toward a decrease in the production of proinflammatory ARA eicosanoids and oxidative stress biomarkers from EPA and DHA. In addition, the ability of 1:1 and 2:1 fish oil diets to reduce lipid mediator levels was in concurrence with the protective effect exerted by decreasing inflammatory markers as ω-6/ω-3 ratio in plasma and membranes. It was also highlighted the effect of a higher DHA amount in the diet reducing the healthy benefits described in terms of inflammation and oxidative stress. Results support the antiinflammatory and antioxidative role of fish oils and, particularly, the effect of adequate proportions EPA:DHA.

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Section: Resultssupporting

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Healthy effect of different proportions of marine ω-3 PUFAs EPA and DHA supplementation in Wistar rats: Lipidomic biomarkers of oxidative stress and inflammation

Dasilva

Pazos

García-Egido

et al. 2015

The Journal of Nutritional Biochemistry

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“…Omega-3 PUFA administration has also been shown to confer protection against hepatic (Kim et al 2013), renal (Ashtiyani et al 2012), intestinal (Arisue et al 2012, Brahmbhatt et al 2013, cerebral (Pan et al 2009), pulmonary (Lee et al 2008), and myocardial (ZeghichiHamri et al 2010, Gao et al 2011) IR injury.…”

Section: Discussionmentioning

confidence: 99%

Maternal omega-3 fatty acid intake increases placental labyrinthine antioxidant capacity but does not protect against fetal growth restriction induced by placental ischaemia–reperfusion injury

Jones¹,

Mark²,

Waddell³

2013

Reproduction

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Placental oxidative stress plays a key role in the pathophysiology of several placenta-related disorders. Oxidative stress occurs when excess reactive oxygen species (ROS) damages cellular components, an outcome limited by antioxidant enzymes; mitochondrial uncoupling protein 2 (UCP2) also limits ROS production. We recently reported that maternal dietary omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation reduced placental oxidative damage and enhanced fetal and placental growth in the rats. Here, we examined the effect of n-3 PUFAs on placental antioxidant defences and whether n-3 PUFA supplementation could prevent growth restriction induced by placental ischaemia-reperfusion (IR), a known inducer of oxidative stress. Rats were fed either standard or high-n-3 PUFA diets from day 1 of pregnancy. Placentas were collected on days 17 and 22 in untreated pregnancies (termZday 23) and at day 22 following IR treatment on day 17. Expression of several antioxidant enzyme genes (Sod1, Sod2, Sod3, Cat, Txn1 and Gpx3) and Ucp2 was measured by quantitative RT-PCR in the placental labyrinth zone (LZ) and junctional zone (JZ). Cytosolic superoxide dismutase (SOD), mitochondrial SOD and catalase (CAT) activities were also analyzed. Maternal n-3 PUFA supplementation increased LZ mRNA expression of Cat at both gestational days (2-and 1.5-fold respectively; P!0.01) and female Sod2 at day 22 (1.4-fold, P!0.01). Cytosolic SOD activity increased with n-3 PUFA supplementation at day 22 (1.3-fold, P!0.05). Sod1 and Txn1 expression decreased marginally (30 and 22%, P!0.05). JZ antioxidant defences were largely unaffected by diet. Despite increased LZ antioxidant defences, maternal n-3 PUFA supplementation did not protect against placental IR-induced growth restriction of the fetus and placental LZ.

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“…Numerous studies demonstrate that dietary or pharmaceutical supplementation with EPA and/or DHA ameliorates oxidative stress by decreasing the levels of iNOS, nitric oxide, nitrous oxide (N 2 O), prostaglandin E2 (PGE2), creatinine, MDA, 4-HNE, IL-1β, TNF-α, IL-6 and COX-2 while upregulating the levels of superoxide dismutase (SOD) and catalase (CAT) [187][188][189][190].…”

Section: Oandns and The Plasma Membranementioning

confidence: 99%

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders

Morris¹,

Walder

Puri

et al. 2015

Mol Neurobiol

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Oxidative and nitrosative stress (O&NS) is causatively implicated in the pathogenesis of Alzheimer's and Parkinson's disease, multiple sclerosis, chronic fatigue syndrome, schizophrenia and depression. Many of the consequences stemming from O&NS, including damage to proteins, lipids and DNA, are well known, whereas the effects of O&NS on lipoprotein-based cellular signalling involving palmitoylation and plasma membrane lipid rafts are less well documented. The aim of this narrative review is to discuss the mechanisms involved in lipid-based signalling, including palmitoylation, membrane/lipid raft (MLR) and n-3 polyunsaturated fatty acid (PUFA) functions, the effects of O&NS processes on these processes and their role in the abovementioned diseases. S-palmitoylation is a post-translational modification, which regulates protein trafficking and association with the plasma membrane, protein subcellular location and functions. Palmitoylation and MRLs play a key role in neuronal functions, including glutamatergic neurotransmission, and immune-inflammatory responses. Palmitoylation, MLRs and n-3 PUFAs are vulnerable to the corruptive effects of O&NS. Chronic O&NS inhibits palmitoylation and causes profound changes in lipid membrane composition, e.g. n-3 PUFA depletion, increased membrane permeability and reduced fluidity, which together lead to disorders in intracellular signal transduction, receptor dysfunction and increased neurotoxicity. Disruption of lipid-based signalling is a source of the neuroimmune disorders involved in the pathophysiology of the abovementioned diseases. n-3 PUFA supplementation is a rational therapeutic approach targeting disruptions in lipid-based signalling.

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Protective effects of dietary EPA and DHA on ischemia–reperfusion-induced intestinal stress

Cited by 34 publications

References 48 publications

Healthy effect of different proportions of marine ω-3 PUFAs EPA and DHA supplementation in Wistar rats: Lipidomic biomarkers of oxidative stress and inflammation

Healthy effect of different proportions of marine ω-3 PUFAs EPA and DHA supplementation in Wistar rats: Lipidomic biomarkers of oxidative stress and inflammation

Maternal omega-3 fatty acid intake increases placental labyrinthine antioxidant capacity but does not protect against fetal growth restriction induced by placental ischaemia–reperfusion injury

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders

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