Cytokine distribution in mothers and breastfed children after omega-3 LCPUFAs supplementation during the last trimester of pregnancy and the lactation period: A randomized, controlled trial.

OBJECTIVE: To determine whether maternal diet supplementation with omega-3 long chain polyunsaturated fatty acids (omega-3 LC-PUFAs) during the last trimester of pregnancy and the breastfeeding period influences the levels of inflammatory cytokines in mother and infants. MATERIAL AND METHOD: This registered, double-blind randomized study included 46 pregnant women, who were randomly allocated to either an experimental group receiving 400mL/day of a fish oil-enriched dairy drink [320mg docosahexaenoic acid (DHA) + 72mg eicoapentaenoic acid] (FO group, n = 24) or to a control group receiving 400mL/day of a non-supplemented dairy drink (CT group, n = 22), from week 28 of pregnancy until the fourth month of lactation. During the study, maternal dietary patterns were monitored by a nutritionist, who encouraged compliance with current recommendations of fatty acids intake. DHA concentrations and cytokine levels (GM-CSF, IL-2, IL-4, IL-6, IL-10, INF-γ and TNF-α) were measured in maternal plasma at the moment of recruitment and in maternal (n = 46) and infant (n = 46) plasma at birth and 2.5 months after birth. RESULTS: Maternal plasmatic IL-4 levels were higher in FO than in CT subjects (p = 0.009). Additionally, a tendency was observed to higher IL-10 and IL-2 in the FO group. Plasmatic IL-6 however, was higher in CT mothers (p = 0.001). TNF-α was higher in CT infants at birth and 2.5 months after birth (p = 0.005). An analysis of possible relationships between DHA and the concentrations of different cytokines revealed negative correlation between maternal plasmatic IL-6 and DHA (higher plasmatic DHA corresponded to lower IL-6). CONCLUSIONS: Maternal dietary omega-3 LC-PUFAs supplementation during critical periods like pregnancy, lactation and early newborn development may influence the levels of certain inflammatory cytokines, reducing pro-inflammatory cytokines and promoting an anti-inflammatory "environment".

Olive oil and mitochondrial oxidative stress.

This review summarizes studies on the role of olive oil intake in the prevention and attenuation of mitochondrial oxidative stress derived from several situations such as ageing, physical exercise, treatment with adriamycin or intake of thermally oxidised oils. After more than fifteen years of studies on these issues, results have demonstrated that under different models of oxidative stress the regular intake of virgin olive oil as dietary fat is able to attenuate or increase free radical production at the mitochondrial level to a lower extent than when n-6 polyunsaturated oils are used. In the same way, virgin olive oil leads to better function of the mitochondrial electron transport chain.

Dietary fat type and regular exercise affect mitochondrial composition and function depending on specific tissue in the rat.

Physical exercise and fatty acids have been studied in relation to mitochondrial composition and function in rat liver, heart, and skeletal muscle. Male rats were divided into two groups according to dietary fat type (virgin olive and sunflower oils). One-half of the animals from each group were subjected to a submaximal exercise for 8 weeks; the other half acted as sedentary controls. Coenzyme Q, cytochromes b, c + c1, a + a3 concentrations, and the activity of cytochrome c oxidase were determined. Regular exercise increased (P < 0.05) the concentration of the above-mentioned elements and the activity of the cytochrome c oxidase by roughly 50% in liver and skeletal muscle. In contrast, physical exercise decreased (P < 0.05) cytochrome c oxidase activity in the heart (in micromol/min/g, from 8.4+/-0.1 to 4.9+/-0.1 in virgin olive oil group and from 9.7+/-0.1 to 6.7+/-0.2 in sunflower oil animals). Dietary fat type raised the levels of coenzyme Q, cytochromes, and cytochrome c oxidase activity in skeletal muscle (P < 0.05) among the rats fed sunflower oil. In conclusion, dietary fat type, regular exercise, and the specific tissue modulate composition and function of rat mitochondria.

Virgin olive oil and coenzyme Q10 protect heart mitochondria from peroxidative damage during aging.

The mitochondrial theory of aging suggests that this phenomenon is the consequence of random somatic mutations in mitochondrial DNA, induced by long-term exposure to free radical attack. There are two potential dietary means of delaying the effects of free radicals on cellular aging, i.e., enrichment of mitochondrial membranes with monounsaturated fatty acids and supplementation with antioxidants. We have performed a preliminary study on male rats, 6 or 12 month old, fed with diets differing in the nature of the fat (virgin olive oil or sunflower oil) and/or with antioxidant supplementation (coenzyme Q10), analysing hydroperoxide and coenzyme Q9 and Q10 in heart mitochondria. Preliminary results allow us to conclude that the CoQ10 dietetic supplementation as well as the enrichment of the cellular membranes with monounsaturated fatty acids, successfully protect mitochondrial membranes from aged rats against the free radical insult.

Relative importance of the saponified and unsaponified fractions of dietary olive oil on mitochondrial lipid peroxidation in rabbit heart.

The effects of four edible oils on lipid peroxidation have been investigated in rabbit heart mitochondrial membranes. The experimental oils (olive oil from the variety "picual", washed olive oil from the variety "picual", olive oil from the variety "arbequina" and high-oleic sunflower oil) had a similar fatty-acid composition, but differed in their unsaponified fraction (polyphenols, tocopherols, and others). The lowest hydroperoxide levels were found with picual and washed picual. No differences in mitochondrial membrane thiobarbituric acid reactive substance (TBARS), alpha-tocopherol concentrations and cytosolic antioxidant enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase) were found, whereas the CoQ10 content correlated inversely with hydroperoxide levels in all groups. These results suggest that mitochondrial membranes with high levels of monounsaturated fatty acids generate low levels of lipid peroxidation. Moreover, the saponified fraction of the experimental diets proved more important in preventing lipid peroxidation than the unsaponified fraction. Lastly, coenzyme Q may help to prevent peroxidative stress damage in rabbit heart mitochondria.