Docosahexaenoic acid enrichment can reduce L929 cell necrosis induced by tumor necrosis factor

Kishida, Etsu; Tajiri, Michiko; Masuzawa, Yasuo

doi:10.1016/j.bbalip.2006.03.023

Cited by 36 publications

(27 citation statements)

References 58 publications

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“…[41][42][43] The mechanism of the protective effect of DPA on prostate cancer may be explained by biochemical processes involving: reduced prostacyclin production, expression of inflammatory genes and TNF-induced necrotic cell death; competition with cycloxygenase 2 (COX2) enzymes resulting to anti-neoplastic activity via proapoptotic pathway; and inhibition of angiogenesis. [44][45][46][47][48][49] Detection of such association may suggest that serum level DPA implicates individual genetic difference in biochemical characteristics of enzymatic activities, which may be further investigated as a probable new serum biomarker for prostate cancer risk assessment in the future.…”

Section: Discussionmentioning

confidence: 99%

The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A Meta-analysis

Chua

Sio²,

Sorongon³

et al. 2013

CUAJ

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Objective:Our objective was to systematically analyze the evidence for an association between serum level long chain omega-3 polyunsaturated fatty acid (n-3 PUFA) and prostate cancer risk from human epidemiological studies. Study Procedures: We searched biomedical literature databases up to November 2011 and included epidemiological studies with description of long chain n-3 PUFA and incidence of prostate cancer in humans. Critical appraisal was done by two independent reviewers. Data were pooled using the general variance-based method with random-effects model; effect estimates were expressed as risk ratio with 95% confidence interval (CI). Heterogeneity was assessed by Chi 2 and quantified by I 2 , publication bias was also determined. Results: In total, 12 studies were included. Significant negative association was noted between high serum level of n-3 PUFA docosapentaenoic acid (DPA) and total prostate cancer risk (RR:0.756; 95% CI 0.599, 0.955; p = 0.019). Likewise, a positive association between high blood level of fish oil contents, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and high-grade prostate tumour incidence (RR:1.381; 95% CI 1.050, 1.817; p = 0.021) was noted; however, this finding was evident only after adjustment was done on interstudy variability through the removal of a lower quality study from the pool. Conclusions: High serum levels of long chain n-3 PUFA DPA is associated with reduced total prostate cancer risk. While high blood level of EPA and DHA is possibly associated with increased high-grade prostate tumour risk.

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Section: Discussionmentioning

confidence: 99%

The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A Meta-analysis

Chua

Sio²,

Sorongon³

et al. 2013

CUAJ

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“…Considerable amounts of ALA were metabolized to longer-chain n-3 fatty acids within the aorta, and a large proportion of ALA was converted to DPA. DPA has been associated with the inhibition of cyclooxygenase 1 activity, a decrease in cellular TNF-␣, and the induction of gene modulatory and anti-inflammatory effects (28,35,36). Additionally, n-3 fatty acids such as EPA and DHA are activators of peroxisome proliferator-activated receptors (PPARs).…”

Section: Discussionmentioning

confidence: 99%

Effects of dietary flaxseed on atherosclerotic plaque regression

Francis

Deniset

Austria

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Francis AA, Deniset JF, Austria JA, LaValleé RK, Maddaford GG, Hedley TE, Dibrov E, Pierce GN. Effects of dietary flaxseed on atherosclerotic plaque regression. Am J Physiol Heart Circ Physiol 304: H1743-H1751, 2013. First published April 12, 2013 doi:10.1152/ajpheart.00606.2012.-Dietary flaxseed can retard the progression of atherosclerotic plaques. However, it remains unclear whether these antiatherogenic effects extend to plaque regression. In the present study, the therapeutic potential of dietary flaxseed on atherosclerotic plaque regression and vascular contractile function was evaluated using a novel rabbit model. Rabbits were randomly assigned to receive either a regular diet for 12 wk (group I) or a 1% cholesterol-supplemented diet for 4 wk followed by a regular diet for 8 wk (group II). The remaining experimental animals were treated as in group II but were fed for an additional 14 wk with either a regular diet (group III) or a 10% flaxseed-supplemented diet (group IV). Animals in group II showed clear evidence of plaque growth stabilization. Their vessels also exhibited significantly lower norepinephrine-induced contraction and an impaired relaxation response to acetylcholine compared with animals in group I. Dietary flaxseed supplementation resulted in a significant Ϸ40% reduction in plaque formation (P ϭ 0.033). Animals in both groups II and III displayed improved contraction and endothelium-dependent vessel relaxation. Dietary flaxseed is a valuable strategy to accelerate the regression of atherosclerotic plaques; however, flaxseed intervention did not demonstrate a clear beneficial effect on the vessel contractile response and endothelium-dependent vasorelaxation. atherosclerosis; flaxseed; heart disease; regression; vascular contractile function CARDIOVASCULAR DISEASE (CVD) is currently the leading cause of mortality worldwide. Its prevalence continues to increase despite improved treatments for atherosclerosis and will reach epidemic proportions within a decade due to the escalating predominance of sedentary, unhealthy lifestyles (32, 51, 52). Atherosclerosis is orchestrated by a complex array of molecular and cellular events commencing after endothelial injury. The resultant plaques may continue to progress, ultimately causing acute events such as myocardial infarction and stroke (23,32). Recently, it has been shown that atherosclerotic plaques are highly dynamic and that their progression can be slowed, stopped, and even reversed by drug intervention (6,18,43). For example, aggressive risk modification with statin drug therapy can remove lipids and necrotic material, restore endothelial function and viability, and prevent vascular smooth muscle cell proliferation and phenotype reversal, three processes involved in atherosclerotic plaque formation (18, 43).Akin to pharmaceuticals, functional foods can also be used to prevent and treat CVD. A functional food has a similar appearance to or may be a conventional food and may be consumed as part of a normal diet to have physiological benefits and/...

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“…The sensitizing effect of DHA was associated with stimulation of oxidative metabolism and proapoptotic events at the level of mitochondria. On the other hand, a protective role of DHA against various cell death types such as apoptosis and necrosis triggered by TNF-α has been reported in other cell types such as human monocytes or fibrosarcoma, respectively 150 . Based on these results, the modulatory effect of DHA on death ligand-induced apoptosis appears to depend significantly on the cell type (tissue of origin, normal/cancer) and its genetic background.…”

Section: Interaction Of Dha With Butyratementioning

confidence: 99%

Docosahexaenoic fatty acid (DHA) in the regulation of colon cell growth and cell death: A review

Skender¹,

Vaculová²,

Hofmanová³

2012

BIOMED PAP

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Background. Experimental, epidemiological and clinical data substantiate the beneficial role of n-3 polyunsaturated fatty acids (PUFAs) in preventing inflammation and cancer of the colon. This review covers the unsaturated docosahexaenoic fatty acid (DHA), describes some of its important cellular and molecular mechanisms, its interaction with another dietary lipid, butyrate and with endogenous apoptotic regulators of the tumour necrosis factor (TNF) family. We also discuss the clinical impact of this knowledge and the use of these lipids in colon cancer prevention and treatment. Results. From the literature, DHA has been shown to suppress the growth, induce apoptosis in colon cancer cells in vitro and decrease the incidence and growth of experimental tumours in vivo. Based on these data and our own experimental results, we describe and discuss the possible mechanisms of DHA anticancer effects at various levels of cell organization. We show that DHA can sensitize colon cancer cells to other chemotherapeutic/chemopreventive agents and affect the action of physiological apoptotic regulators of the TNF family. Conclusion. Use of n-3 PUFAs could be a relatively non-toxic form of supportive therapy for improving colon cancer treatment and slowing down or preventing its recurrence. However, it is necessary to use them with caution, based on solid scientific evidence of their mechanisms of action from the molecular to the cellular and organism levels.

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Docosahexaenoic acid enrichment can reduce L929 cell necrosis induced by tumor necrosis factor

Cited by 36 publications

References 58 publications

The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A Meta-analysis

The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A Meta-analysis

Effects of dietary flaxseed on atherosclerotic plaque regression

Docosahexaenoic fatty acid (DHA) in the regulation of colon cell growth and cell death: A review

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