A study of essential fatty acid metabolism as a precursor of prostaglandin in collagen disease.
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Linoleic, linolenic and arachidonic acids, dispersed at a concentration of 2.5 x 10-3 M in an aqueous media pH 7.3, exhibited increasing of their autoxidation rate in presence of 1.5 x 10-5M alpha-tocopherol or more. Cosidering linolenic and arachidonic acids, prooxidant effect increased with alpha-tocopherol level while for linoleic acid this effect was similar with all alpha-tocopherol concentrations. During the prooxidant reaction, alpha-tocopherol was rapidly oxidized. Its oxidation rate depended on hydroperoxides level. It was the most important in presence of arachidonic acid. After 24 hours, alpha-tocopherol was completly oxidized whatever its initial concentration and the type of the fatty acid. Two oxidation products have been identified : alpha-tocopherylquinone for the most part and a dimer of alpha-tocopherol which was detected at the beginning of the reaction.
A balanced intake of alimentary lipids is necessary for calcium and phosphorus absorption, as for growth and calcification of bone. In lipid deprivation or excess, important disorders of phospho-calcic metabolism appear particularly in young growing subjects. The qualitative content of ingested fats has, too, a great influence : lipids containing short and medium-chain fatty acids, essential fatty acids and oleic acid stimulate calcium absorption. An excess of long chain and saturated lipids, or intake of erucic acid depress calcium absorption and retention. These facts are possible pathophysiological mechanisms in human disorders: The so-called humanized milks are close to human milk regarding their capacity of stimulation of phospho-calcic absorption and growth. In these milks, oleic and linoleic triglyceride level must be increased. In adult pathology, lipidic deficiency of steatorrhea is partially responsible for calcium and vitamin D malabsorption. Conversely, lipid-calcium interactions are not one-way, and an elevated dietary calcium depresses saturated lipid absorption, and has a hypolipemic action interesting in prevention of atherosclerosis of aged patients.
EFAs have shown promising anti-tumour effects in cell culture studies and in animal models. However, it is also clear that in man EFAs can have marked immunomodulatory effects, in particular, inhibiting certain aspects of host anti-tumour defence mechanisms (natural cytotoxicity and cytokine production). Further careful studies are required to evaluate more precisely the role of EFAs in the treatment of malignant disease in man.
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Plasma cholesterol ester and triglyceride fatty acid compositions of 38 singleton deliveries (23-42 wk), three twins (32, 39, and 40 wk), and their mothers were investigated. No gestational age-dependent changes occurred in maternal fatty acid compositions. Long-chain polyunsaturated fatty acids in fetal cholesterol esters and triglycerides were higher, and their precursors (18:2c,omega 6 and 18:3c,omega 3) were lower than those in corresponding maternal lipid classes. Except for 22:6c,omega 3,20:2c,omega 6, and 22:5c,omega 6, all long-chain polyunsaturated fatty acids in fetal triglycerides increased with advancing gestation. Fetal triglyceride 22:6c,omega 3/22:5c,omega 3 ratio decreased, whereas 22:5c,omega 6/22:4c,omega 6 remained constant. Fetal cholesterol ester and triglyceride 20:3c,omega 9 contents were higher than those of corresponding maternal fractions and did not change with gestation. Triglyceride 18:2c,omega 6 contents of babies with gestational ages of more than 34 wk were linearly related to those of their mothers. The data suggest that increasing triglyceride long-chain polyunsaturated fatty acid content with advancing gestation is partially caused by delta 6- and delta 5-desaturase maturation in the liver. Constancy of 22:6c,omega 3 and 22:5c,omega 6/22:4c,omega 6 and decrease of 22:6c,omega 3/22:5c,omega 3 in triglycerides may point to low hepatic delta 4-desaturation. Transplacental transport of 20:3c,omega 9, following by fetal conservation, should be considered. High 18:2c,omega 6 and low 18:3,omega 3 intakes by the mother may unfavorably influence fetal production of 22:6c,omega 3 in the liver. Because of low hepatic delta 4-desaturation capacity the influence may be small, however.
The authors review the origins and the metabolism of omega-6 and omega-3 fatty acids and particularly consider the implications of desaturase's deficiency and of the usual imbalanced supply of fatty acids in the diet of children. The peculiarity of the fatty acids is to be, while proteins express the genome, the expression of the diet on the cell's membranes, with a subtle influence of an enzyme's equipment varying during the life. All that gains an extraordinary relief, because the omega-6 and omega-3, and constituents of the membranes, are precursors of different series of prostaglandins, which are wholebody mediators of multiple phenomenons like inflammation, immunity, allergy, platelet aggregation, ecc. The authors point how a balanced diet or a supplementation with omega-3, omega-6 and PUFA can help a good development especially of the nervous tissue and of the mucosal barrier. Furthermore modulating the above physiopathological mechanism, also in children could influence recurrent and chronic diseases.
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