N-3 LC-PUFAs

Whole-body fatty-acid-balance methodology exploits the fact that in the absence of other n-3 PUFA, the diet is the only source of a-linolenate besides what is already present in the body. By comparing a-linolenate intake to accumulation of the sum of all n-3 PUFA determined over a balance period of several days to several weeks (deducting excretion and conversion to n-3 LC-PUFA). one can calculate a-linolenate disappearance or P-oxidation by difference. The advantages of the whole-body balance method are that (1) it reflects metabolism in the whole body rather than in an isolated tissue or subcel-lular compartment and (2) during energy deficit, this method alone can provide an estimate of a-linolenate oxidation derived from existing body stores as well as from the diet. 

These data do not prove that sufficient docosahexaenoate cannot be made from a-linolenate. Rather, they establish that <10% of dietary a-linolenate is normally available for docosahexaenoate synthesis in the suckling rat. Results obtained using whole-body-balance methodology see Section 2) suggest that this 10% availability of a-linolenate for synthesis of n-3 LC-PUFA decreases substantially during undemutrition. 

The studies described here suggest that only about 10% of a-linolenate consumed by suckling rats is available for esterification or conversion to n-3 LC-PUFA. Although this... 

Due to a growing interest in the bioactive properties of n-3 LC-PUFAs, there is an increasing demand for purified concentrates for use as dietary supplements and in functional foods however, it is believed that traditional sources will be insufficient in meeting this demand (Bajpai and Bajpai, 1993 Lewis et al, 1999). In addition to development of improved methods of omega-3 extraction from fish oils, a possible solution is the use of alternative. 

The n-3 LC-PUFA have a beneficial effect on plasma triglycerides, high blood pressure, whole-blood viscosity, and platelet function they inhibit the expression of cell-adhesion molecules, shift the eicosanoid profile to one of lesser thrombotic and inflammatory potential, improve vessel-wall compliance, and have antiarrhythmic potential (1,2). A number of intervention trials have associated the consumption of fish with decreased mortality from CVD (3-5). High doses of fish oil eliminate both vascular thrombus as well as vascular lesion formation (6). In men who had had a recent myocardial infarction, low-dose dietary supplementation with n-3 LC-PUFA, in addition to the recommended secondary prevention treatments, reduced by 45% the risk of sudden cardiac death, but not the risk of nonfatal myocardial infarction (7). It has been shown to mitigate the course of coronary atherosclerosis in humans (8). 

The susceptibility of LDL toward oxidation can be tested in vitro and ex vivo. When LDL are isolated from human plasma and exposed to free copper ions, the amount or velocity of peroxides formed is measured. It is not until aU of the available vitamin E and other antioxidants have been consumed that LDL peroxidation occurs. In line with that theory, many studies have reported that higher intakes of PUFA (linolenate and n-3 LC-PUFA) increase LDL susceptibility to ex vivo oxidation (20-26). 

It has to be remembered that the results of in vitro and ex vivo studies on the effect of n-3 LC-PUFA on LDL oxidation are equivocal. Many studies showed either no LDL oxidation under fish oil (27-32), or even a decrease in the rate and the extent of oxidation (33,34). These seemingly contradictory findings may be related to the methodology of measuring LDL oxidation, as well as to the actual variable chosen to evaluate LDL susceptibility. To what extent oxidative susceptibility of LDL measured ex vivo reflects oxidative susceptibility in vivo is unknown. 

Overlooked or largely ignored have been studies demonstrating an antioxidant effect of n-3 PUFA in vitro, in various animal oxidant stress models, and in humans. Table 1 lists the many reports describing effects of n-3 LC-PUFA on ROS-mediated events, ROS biomarkers, and antioxidative defense systems, which can be interpreted in terms of an antioxidant activity of n-3 LC-PUFA. 

Inadequate levels of vitamin E and other antioxidants will lead to the loss of PUFA through oxidation and to oxidative damage of key biomolecules. The latter has become accepted as a probable factor in atherogenesis, endothelial dysfunction, and myocardial ischemia, whereas it is rarely considered that the loss of n-3 LC-PUFA could be as impor-... 

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