Dietary long-chain omega-3 fatty acids of marine origin: a comparison of their protective effects on coronary heart disease and breast cancers.
The relationship between high fish consumption and low mortality following coronary heart disease (CHD) and low incidence of breast cancer was first mentioned 3 decades ago. The fishes of interest are rich in omega-3 long-chain polyunsaturated fatty acids (omega-3 LC-PUFAs), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which could be the active nutrients. The current consensus about cardioprotection is that omega-3 LC-PUFAs would mainly exert antiarrhythmic effects. One of the proposed mechanisms is that circulating non-esterified LC-PUFAs partition into cardiac cells membrane phospholipids and exert a direct effect on ionic channels and/or modify intracellular calcium homeostasis. In another hypothesis, changes in the metabolism of phosphoinositides would be involved and lead to the differential activation of PKC isoforms. As compared to the mechanisms proposed for the cardioprotective effects of omega-3 LC-PUFAs, less is known about the molecular mechanisms involved in breast cancers prevention. Some proposed mechanisms such as the modulation of phosphoinositides metabolism and/or modulation of intracellular calcium homeostasis, are common to both pathologies. Other hypotheses involve the alteration of the cellular redox status induced by highly peroxidizable polyunsaturated fatty acids (FA), or the modulation of gene expression, both phenomena being tightly linked to apoptosis. In this review, we report and compare some proposed mechanisms for the involvement of omega-3 LC-PUFAs in both cardiac and breast cancer protection. Deliberately, we chose to discuss only the mechanisms, which are less described in other reviews such as ionic channels in cancer, calcium homeostasis, PKC activation or matrix metalloproteinases in both cancer and cardiac models. The leitmotiv along this review is that cardio- and cancero-protective effects use common pathways. Comparison of the cellular effects might therefore help to highlight the "protective" pathways.
Judé
Sébastien
S
Centre de Recherches Biologiques, Chemin de Montifault, 18800 Baugy, France.
Roger
Sébastien
S
Martel
Eric
E
Besson
Pierre
P
Richard
Serge
S
Bougnoux
Philippe
P
Champeroux
Pascal
P
Le Guennec
Jean-Yves
JY
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001145:Arrhythmias, Cardiac / Q000178:diet therapy / Q000517:prevention & control; D001943:Breast Neoplasms / Q000178:diet therapy / Q000517:prevention & control*; D003327:Coronary Disease / Q000178:diet therapy / Q000517:prevention & control*; D004041:Dietary Fats / Q000378:metabolism / Q000627:therapeutic use; D004281:Docosahexaenoic Acids / Q000378:metabolism* / Q000627:therapeutic use; D015118:Eicosapentaenoic Acid / Q000378:metabolism* / Q000627:therapeutic use; D004789:Enzyme Activation; D005399:Fishes / Q000378:metabolism; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D020782:Matrix Metalloproteinases / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism
D004041:Dietary Fats; D007473:Ion Channels; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D011493:Protein Kinase C; D020782:Matrix Metalloproteinases