Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis

Peskin, Brian Scott

doi:10.1155/2014/495761

Cited by 7 publications

(4 citation statements)

References 74 publications

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“…It is evident that n-3 PUFAs induce apoptosis in cancer cells by triggering excessive ROS production and inducing autophagy [ 34 , 35 ]. Having more unsaturated double bonds and bis -allylic hydrogens than monounsaturated fatty acid, n-3 PUFAs are much more prone to spontaneous oxidation and result in an increase in ROS production [ 36 ]. Compared to normal cells, cancer cells have higher levels of mitochondrial ROS generation for cellular proliferation and tumorigenesis, the ROS products further attack n-3 PUFAs and cause more lipid peroxidation and lead to apoptosis in cancer cells [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

Hsu

Chen

2014

J Biomed Sci

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BackgroundUse of the chemotherapeutic drug doxorubicin (DOX) is associated with serious cardiotoxicity, as it increases levels of reactive oxygen species (ROS). N-3 polyunsaturated fatty acid dietary supplements can be of benefit to patients undergoing cancer therapy. The aims of this study were to determine whether DOX-induced cardiotoxicity is related to mitochondrial uncoupling proteins and whether eicosapentaenoic acid (EPA, C20:5 n-3) or docosahexaenoic acid (DHA, C22:6 n-3) affects DOX-induced cardiomyocyte toxicity.ResultsTreatment of H9C2 cells with DOX resulted in decreased cell viability and UCP2 expression. Treatment with 100 μM EPA or 50 μM DHA for 24 h resulted in a maximal mitochondria concentration of these fatty acids and increased UCP2 expression. Pretreatment with 100 μM EPA or 50 μM DHA prevented the DOX-induced decrease in UCP2 mRNA and protein levels, but these effects were not seen with EPA or DHA and DOX cotreatment. In addition, the DOX-induced increase in ROS production and subsequent mitochondrial membrane potential change (∆ψ) were significantly attenuated by pretreatment with EPA or DHA.ConclusionEPA or DHA pre-treatment inhibits the DOX-induced decrease in UCP2 expression, increase in ROS production, and subsequent mitochondrial membrane potential change that contribute to the cardiotoxicity of DOX.Electronic supplementary materialThe online version of this article (doi:10.1186/s12929-014-0101-3) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

Hsu

Chen

2014

J Biomed Sci

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“…Since the 1930s essential roles were assigned to the n-3 polyunsaturated fatty acids (PUFAs), because their lack in the diet gave rise to not yet known forms of deficiency diseases at the time [96]. There is a lot of literature that speaks of the various beneficial effects of PUFAs such as protective effects against cardiovascular disease, inflammation, and cancer [97,98], although there are now several articles that challenge the beneficial effects of these fatty acids [99].…”

Section: Endocannabinoids Systemmentioning

confidence: 99%

Endocannabinoids, Related Compounds and Their Metabolic Routes

et al. 2014

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Endocannabinoids are lipid mediators able to bind to and activate cannabinoid receptors, the primary molecular targets responsible for the pharmacological effects of the Δ 9 -tetrahydrocannabinol. These bioactive lipids belong mainly to two classes of compounds: N-acylethanolamines and acylesters, being N-arachidonoylethanolamine (AEA) and 2-arachidonoylglycerol (2-AG), respectively, their main representatives. During the last twenty years, an ever growing number of fatty acid derivatives (endocannabinoids and endocannabinoid-like compounds) have been discovered and their activities biological is the subject of intense investigations. Here, the most recent advances, from a therapeutic point of view, on endocannabinoids, related compounds, and their metabolic routes will be reviewed.

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“…Unsurprisingly, of late, DHA as an anti-growth factor is found to counter hypertension [74]. Having said this, and understanding the prosurvival mechanisms targeted by DHA from cancer, it is to be anticipated that DHA may well fail in terms of prevention of heart disease overall -a conclusion that is becoming apparent [75]-hence limiting DHA as a therapy in itself. This may be understood in light of the notion that DHA potentially targets prosurvival mechanisms in cardiomyocytes, thus countering any potential benefit to be gained from its vascular effects.…”

Section: Addressing Therapeuticsmentioning

confidence: 99%

Viewing cancer pathophysiology as a lead in understanding cardiac and vascular disease mechanisms

Loudon¹

2014

Cardio Vasc Syst

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This article describes how understanding mechanisms used by cancer cells-both prosurvival (oncogenic) and pro-apoptotic (tumour suppression)-sheds light on important 'cues' for prosurvival and apoptotic pathways employed in the cardiac and vascular system. Commencing with the mevalonate pathway, numerous examples are presented whereby cancer oftentimes foretells an understanding of relevant mechanisms for cardiology. Pathologies such as cardiomyopathies including heart failure, hypertension/ vascular dysfunction, and reaction to ischaemic-reperfusion injury are discussed. Key features emerge in terms of homeostasis within the cardiac and vascular system and the observation that cardiac pathologies do not present in mere isolation but as co-morbidities. Mechanisms resulting in such pathologies are revealed by considering prosurvival versus pro-apoptotic imbalance (homeostatic disturbance). Overall, one may gain an improved foreknowledge of such mechanisms behind these important regulatory paths in cardiology from studying cancer molecular mechanisms.

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Why Fish Oil Fails: A Comprehensive 21st Century Lipids-Based Physiologic Analysis

Cited by 7 publications

References 74 publications

N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

N-3 polyunsaturated fatty acids decrease levels of doxorubicin-induced reactive oxygen species in cardiomyocytes -- involvement of uncoupling protein UCP2

Endocannabinoids, Related Compounds and Their Metabolic Routes

Viewing cancer pathophysiology as a lead in understanding cardiac and vascular disease mechanisms

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