Background: Lycopene, the main carotenoid in tomato, has been shown to be a potent antioxidant in vitro. However, there is no significant evidence of its antioxidant action in vivo. Objective: We evaluated the effect of tomato intake on plasma carotenoid concentrations and lymphocyte resistance to oxidative stress. Design: Ten healthy women (divided into 2 groups of 5 subjects each) ate a diet containing tomato purée (providing 16.5 mg lycopene) and a tomato-free diet for 21 d each in a crossover design. Before and after each diet period, plasma carotenoid concentrations and primary lymphocyte resistance to oxidative stress (evaluated by means of single-cell gel electrophoresis) were analyzed. Results: After the first 21-d experimental period, total plasma lycopene concentrations increased by 0.5 mol/L (95% CI: 0.14, 0.87) in the group that consumed the tomato diet and decreased by 0.2 mol/L (95% CI: Ϫ0.11, Ϫ0.30) in the group that consumed the tomato-free diet (P < 0.001). Tomato consumption also had an effect on cellular antioxidant capacity: lymphocyte DNA damage after ex vivo treatment with hydrogen peroxide decreased by 33% (95% CI: 0.8%, 61%; P < 0.05) and by 42% (95% CI: 5.1%, 78%; P < 0.05) in the 2 groups of subjects after consumption of the tomato diet. Conclusion:The consumption of tomato products may reduce the susceptibility of lymphocyte DNA to oxidative damage. Am J Clin Nutr 1999;69:712-8.

To test the hypothesis that fish oil supplementation can inhibit the expression of functionally associated molecules on the surface of human blood monocytes, we randomly assigned 12 healthy adults to receive either an n-3 polyunsaturated fatty acid-rich fish oil supplement for 21 d or to receive no supplement. The percentage of monocytes expressing major histocompatibility complex (MHC) class II molecules (HLA-DR, -DP, and -DQ), intercellular adhesion molecule-1, and leukocyte-function-associated antigen-1, and the intensity of expression of each molecule were quantified before and after the study period. Monocytes were examined immediately after blood sampling and again after incubation in serum-free culture medium for 24 h in the presence of interferon-gamma to up-regulate expression of MHC class II molecules by the monocytes. The intensity of expression of all the monocyte surface molecules examined was significantly reduced after fish oil supplementation (P < 0.025), although there was no change in the percentage of monocytes expressing each molecule. After incubation with interferon-gamma, there was a similar inhibition of surface molecule expression (with the exception of HLA-DQ) by monocytes from the fish oil-supplemented group, and there was a reduction in the percentage of monocytes expressing both HLA-DR and -DP molecules (P < 0.025). No significant changes were observed in the reference group. Dietary supplementation with fish oil can inhibit the expression of surface molecules involved in the function of human antigen-presenting cells, a potential mechanism by which n-3 fatty acids may suppress cell-mediated immune responses.

Diets rich in (n-3) polyunsaturated fatty acids (PUFA) are associated with suppression of the immune system, but the mechanisms are unclear. Specific immune responses are initiated by antigen-presenting cells. This study examines the in vitro effect of the (n-3) PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the expression of cell surface molecules required for normal antigen-presenting cell function on human blood monocytes. Monocytes were incubated with or without EPA or DHA for 48 h at 37 degrees C. Following incubation, expression of major histocompatibility complex (MHC) class II molecules (HLA-DR, -DP and -DQ) and adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and leucocyte function associated antigen-1] was quantified by flow cytometry. In the presence of EPA alone there was a significantly lower median intensity of expression of HLA-DR and ICAM-1 relative to incubations without EPA. In contrast, significantly greater median intensities of expression of HLA-DR and -DP were observed following incubation with DHA. In parallel experiments, where monocytes were simultaneously activated by the addition of interferon-gamma to the cultures, median expression intensities of HLA-DR, -DP and ICAM-1 were significantly lower in the presence of either EPA or DHA compared with incubations without the (n-3) PUFA. These findings support previous animal studies that suggest that (n-3) PUFA can influence immune reactivity by modulating antigen-presenting cell function.

Diets rich in n-3 polyunsaturated fatty acids (PUFAs) are associated with suppression of cell-mediated immune responses, but the mechanisms are unclear. We hypothesized that n-3 PUFAs can inhibit the function of human antigen-presenting cells. A prerequisite for this role of blood monocytes is the cell surface expression of major histocompatibility complex (MHC) class II molecules [human leukocyte antigen (HLA)-DR, -DP, and -DQ], aided by the presence of intercellular adhesion molecule-1 (ICAM-1) and leukocyte function associated antigens 1 and 3. We showed previously that the n-3 PUFA eicosapentaenoic acid (EPA) inhibits the expression of HLA-DR on unstimulated human monocytes in vitro, but that docosahexaenoic acid (DHA) enhances its expression. However, both n-3 PUFAs suppress the expression of HLA-DR, HLA-DP, and ICAM-1 on interferon-gamma-activated monocytes. We also established that dietary fish-oil supplementation can inhibit the expression of these surface molecules on circulating human monocytes. We subsequently showed that when EPA and DHA were combined in the same ratio as is commonly found in fish-oil-supplement capsules (3:2), there was no significant effect in vitro on the expression of HLA-DR on unstimulated monocytes, but the expression on activated monocytes remained significantly inhibited. In the same in vitro system, the ability of activated monocytes to present antigen to autologous lymphocytes was significantly reduced after culture with the combined n-3 PUFAs. These findings provide one potential mechanism for the beneficial effect of fish oil in the treatment of rheumatoid arthritis, a disorder associated with elevated expression of MHC class II and adhesion molecules on monocytes present within affected joints.