Evidence indicates that principal features of the membrane involve structural organization of lipids in the form of a bilayer with functional proteins either bound to the bilayer surface or inserted into the bilayer and interacting within specific domains in the lipid milieux. In homeotherms, intrinsic and extrinsic factors apparently form the basis for determination of membrane lipid composition and thus membrane physicochemical properties. Moreover, many intrinsic metabolic controls, such as fatty acid desaturation and phospholipid biosynthesis, may be attenuated by change in the nature of the extrinsic or dietary influence. This review will focus on the role of dietary fat as a determinant of subcellular structural constituents to illustrate that feeding nutritionally adequate diets differing in fatty acid composition can induce physiological transitions in membrane function involving the activity of enzymes responsible for synthesis of membrane constituents, hormone-activated functions and expression of activity in the cell nucleus.

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Menhaden fish oil (FO) containing n-3 fatty acids dramatically extends the life span and delays the onset and progression of autoimmune disease in (NZBxNZW)F1 (B/W) female mice as compared to those fed corn oil (CO) rich in n-6 lipids. As an inefficient antioxidant defense system has been linked to autoimmune diseases, the present study was undertaken to determine whether the protective action of n-3 lipids is mediated through their antioxidant defense system. Weanling B/W mice were fed a nutritionally adequate, semipurified diet containing CO or krill oil (KO) or FO at 10% level (w/w) ad libitum until the mice were 6.5 months old. All diets contained the same level of vitamin E (21.5 mg/100 g diet). We compared the effects of feeding n-6 and n-3 lipids on survival, kidney disease, hepatic microsomal lipid composition, peroxidation, and on the activity and mRNA expression of the antioxidant enzymes catalase, glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) in 6.5-month-old B/W mice. The results showed that when compared to livers from CO-fed mice, livers from KO- and FO-fed mice showed: (i) significantly higher (P < 0.001) activities and expression of CAT, GSH-Px and SOD; (ii) significantly lower (P < 0.001) arachidonic acid (20:4n-6) and linoleic acid (18:2n-6) and higher (P < 0.001) eicosapentaenoic acid (20:5n-3) and docosahexaenoic acid (22:6n-3) levels in hepatic microsomes; and (iii) significantly lower (P < 0.001) estimated peroxidation indices and thiobarbituric acid reactive substances generation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Athletes are exposed to acute and chronic stress that may lead to suppression of the immune system and increased oxidative species generation. In addition, the tendency to consume fewer calories than expended and to avoid fats may further compromise the immune system and antioxidant mechanisms. The exercise stress is proportional to the intensity and duration of the exercise, relative to the maximal capacity of the athlete. Muscle glycogen depletion compromises exercise performance and it also increases the stress. Glycogen stores can be protected by increased fat oxidation (glycogen sparing). The diets of athletes should be balanced so that total caloric intake equals expenditure, and so that the carbohydrates and fats utilised in exercise are replenished. Many athletes do not meet these criteria and have compromised glycogen or fat stores, have deficits in essential fats, and do not take in sufficient micronutrients to support exercise performance, immune competence and antioxidant defence. Either overtraining or under nutrition may lead to an increased risk of infections. Exercise stress leads to a proportional increase in stress hormone levels and concomitant changes in several aspects of immunity, including the following: high cortisol; neutrophilia; lymphopenia; decreases in granulocyte oxidative burst, nasal mucociliary clearance, natural killer cell activity, lymphocyte proliferation, the delayed-type sensitivity response, the production of cytokines in response to mitogens, and nasal and salivary immunoglobulin A levels; blunted major histocompatibility complex II expression in macrophages; and increases in blood granulocyte and monocyte phagocytosis, and pro- and anti-inflammatory cytokines. In addition to providing fuel for exercise, glycolysis, glutaminlysis, fat oxidation and protein degradation participate in metabolism and synthesis of the immune components. Compromising, or overusing, any of these components may lead to immunosuppression. In some cases, supplementation with micronutrients may facilitate the immune system and compensate for deficits in essential nutrients. In summary, athletes should eat adequate calories and nutrients to balance expenditure of all nutrients. Dietary insufficiencies should be compensated for by supplementation with nutrients, with care not to over compensate. By following these rules, and regulating training to avoid overtraining, the immune system can be maintained to minimise the risk of upper respiratory tract infections.

It is clear from our observations that the beneficial effects of FO can be enhanced by the addition of 500 IU of vit-E in the diet. The FO diet containing 500 IU of vit-E may specifically modulate the levels of IL-6, IL-10, IL-12 and TNF-alpha and thereby may delay the onset of autoimmunity in the MRL/lpr mouse model. The observations from this study may form a basis for selective nutrition intervention based on specific fatty acids and antioxidants in delaying the progress of RA.

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