Temporal changes in cerebral antioxidant enzyme activities after ischemia and reperfusion in a rat focal brain ischemia model: effect of dietary fish oil

Choi-Kwon, Smi; Park, Kyung-Ae; Lee, Hee Joo; Park, Myung‐Sook; Lee, Joung Hee; Jeon, Sang Eun; Choe, Myoung Ae; Park, Kyungchan

doi:10.1016/j.devbrainres.2004.05.004

Cited by 66 publications

(46 citation statements)

References 51 publications

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“…EPA and DHA are nutritional antioxidants that decrease cerebral lipid peroxides (Hossain et al 1999;Choin-Kwon et al 2004), with protective effects against neurological and neuropsychiatric disorders (Black et al 1984). Sarsilmaz et al (2003a, b) hypothesized that x-3 EFA may affect the oxidant/antioxidant status of the brain by stabilizing the membrane structures of the brain tissues.…”

Section: Discussionmentioning

confidence: 99%

Effects of ω-3 Essential Fatty Acids (ω-3 EFAs) on Motor Disorders and Memory Dysfunction Typical Neuroleptic-induced: Behavioral and Biochemical Parameter

et al. 2009

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The effects of fish oil supplementation on motor disorders, memory dysfunction, and lipid peroxidation (LP) induced by typical neuroleptics were studied. Wistar rats received a suspension prepared with fish oil containing omega-3 fatty acids, water, and Tween 80 (1%) in the place of drinking water (FO group) or vehicle (C group) for 8 weeks. After 4 weeks of treatment, half of the animals of both groups were treated with haloperidol (H and FO + H groups; experiment 1), fluphenazine (F and FO + F groups; experiment 2), or vehicle (C group), administered once a week (12 mg/kg/im) for 4 weeks, maintaining the treatment with FO. Extrapyramidal motor disorders by haloperidol and fluphenazine were observed by an increase in vacuous chewing movements and catalepsy (P < 0.05). These effects were reduced by FO treatment (P < 0.05). Both neuroleptics displayed impairment in memory retention observed by latency time to find the original location of platform in water-maze task, after 4 days of training performed in the last treatment week. This effect was reduced by FO (P < 0.05) to both haloperidol and fluphenazine treatments. Haloperidol increased the LP in plasma and hippocampus, and these effects were decreased by FO treatment (P < 0.05). Fluphenazine increased the LP in plasma and substantia nigra, which were completely decreased by FO treatment (P < 0.05). The FO decreased the motor disorders, memory dysfunction, and oxidative damage typical neuroleptic-induced. Our results indicate that FO exhibits a neuroprotector role useful on diseases related to oxidative damages, and may be considered in the prevention of motor and memory side effects induced by the antipsychotic treatment.

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Section: Discussionmentioning

confidence: 99%

Effects of ω-3 Essential Fatty Acids (ω-3 EFAs) on Motor Disorders and Memory Dysfunction Typical Neuroleptic-induced: Behavioral and Biochemical Parameter

et al. 2009

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“…In addition, it has been indicated that low levels of DHA in brain are associated with neurodegenerative diseases, such as generalized peroxisomal disorders (12) and Alzheimer's disease (13). Furthermore, DHA supplementation has been shown to alleviate symptoms in some patients with peroxisomal disorders (14), prevent dendritic pathology observed in Alzheimer's disease mouse models (15), and reduce neuronal injury in experimental brain ischemia (16,17). Although all this evidence indicates the beneficial effect of DHA and suggest a requirement of DHA accretion in neuronal cells, underlying mechanisms are not well understood.…”

mentioning

confidence: 99%

Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival

Akbar

Calderón

Zhao

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

404

319

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Phosphatidylinositol 3-kinase [PI (3)K]/Akt signaling is a critical pathway in cell survival. Here, we demonstrate a mechanism where membrane alteration by the n-3 fatty acid status affects Akt signaling, impacting neuronal survival. Docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid highly enriched in neuronal membranes, promotes neuronal survival by facilitating membrane translocation/activation of Akt through its capacity to increase phosphatidylserine (PS), the major acidic phospholipid in cell membranes. The activation of PI (3)K and phosphatidylsinositol triphosphate formation were not affected by DHA, indicating that membrane interaction of Akt is the event responsible for the DHA effect. Docosapentaenoic acid, which replaces DHA during n-3 fatty acid deficiency, was less effective in accumulating PS and translocating Akt and thus less effective in preventing apoptosis. Consistently, in vivo reduction of DHA by dietary depletion of n-3 fatty acids decreased hippocampal PS and increased neuronal susceptibility to apoptosis in cultures. This mechanism may contribute to neurological deficits associated with n-3 fatty acid deficiency and support protective effects of DHA in pathological models such as brain ischemia or Alzheimer's disease

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“…Although EPA and DHA are more easily oxidized compared with arachidonic acid, DHA/EPA supplementation has been associated with the induction of cellular antioxidant responses (57)(58)(59). However, the biochemical pathways responsible for these effects are currently not well understood.…”

Section: Discussionmentioning

confidence: 99%

Novel n-3 Fatty Acid Oxidation Products Activate Nrf2 by Destabilizing the Association between Keap1 and Cullin3

Gao

Wang

Sekhar

et al. 2007

Journal of Biological Chemistry

254

165

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Consumption of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) can mitigate the progression of diseases in which oxidative stress represents a common underlying biochemical process. Nrf2-regulated gene expression regulates detoxification of reactive oxygen species. EPA and DHA were subjected to an in vitro free radical oxidation process that models in vivo conditions. Oxidized n-3 fatty acids reacted directly with the negative regulator of Nrf2, Keap1, initiating Keap1 dissociation with Cullin3, thereby inducing Nrf2-directed gene expression. Liquid chromatography-tandem mass spectrometry analyses of oxidized EPA demonstrated the presence of novel cyclopentenone-containing molecules termed J 3 -isoprostanes in vitro and in vivo and were shown to induce Nrf2-directed gene expression. These experiments provide a biochemical basis for the hypothesis that formation of J-ring compounds generated from oxidation of EPA and DHA in vivo can reach concentrations high enough to induce Nrf2-based cellular defense systems.Eicosapentaenoic acid (EPA, C20:5n-3) 5 and docosahexaenoic acid (DHA, C22:6n-3) are two major components of fish oil. Epidemiological studies and randomized controlled trials have demonstrated that n-3 fatty acid supplementation can reduce sudden cardiac death, nonfatal stroke, and decrease progression of arteriosclerosis (1-3). Dietary supplementation with fish oil also shows promise for suppressing progression of neurodegenerative diseases (4), neuropsychiatric disorders (5), human immunodeficiency virus (6), and diseases of the retina (7). Thus, identifying the molecular mechanism(s) responsible for n-3 fatty acid mitigation of these diverse diseases represents an important and intriguing question.Oxidative stress is a common factor in the etiology of the diseases impacted by DHA and EPA (1, 8 -17). These n-3 fatty acids are very susceptible to free radical oxidation, exceeding that of arachidonic acid (AA) (18 -20). Yet, recent studies have shown that EPA and DHA supplementation reduced urinary F 2 -isoprotane levels, a marker for oxidative stress, as well as enhanced cellular antioxidant defense systems (21-24). Although a reduction of F 2 -isoprostane levels can be attributed, in part, to a decrease in membrane AA content (20,25), the relationship between EPA/ DHA oxidation versus EPA/DHA-mediated induction of antioxidant responses is not well understood.Non-enzymatic free-radical peroxidation of AA results in the formation of multiple stereoisomers of prostaglandin H 2 -like bicyclic endoperoxides that can undergo thiol-mediated reduction to form prostaglandin-like compounds termed F 2 -isoprostanes (F 2 -IsoPs) or rearrangement and reduction to form E 2 -IsoPs, D 2 -IsoPs, and isothromboxanes. E 2 /D 2 -IsoPs can then dehydrate to highly reactive A 2 /J 2 -isoprostanes containing cyclopentenone rings. These compounds readily adduct thiol groups on proteins and have been shown to induce Nrf2/ ARE-directed gene expression (26).NF-E2-related factor 2, Nrf2, is a master transcription factor ...

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Temporal changes in cerebral antioxidant enzyme activities after ischemia and reperfusion in a rat focal brain ischemia model: effect of dietary fish oil

Cited by 66 publications

References 51 publications

Effects of ω-3 Essential Fatty Acids (ω-3 EFAs) on Motor Disorders and Memory Dysfunction Typical Neuroleptic-induced: Behavioral and Biochemical Parameter

Effects of ω-3 Essential Fatty Acids (ω-3 EFAs) on Motor Disorders and Memory Dysfunction Typical Neuroleptic-induced: Behavioral and Biochemical Parameter

Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival

Novel n-3 Fatty Acid Oxidation Products Activate Nrf2 by Destabilizing the Association between Keap1 and Cullin3

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