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In any case, these differences show that their turnover is slower than that of plasma lipids. Nitric oxide is known to favour the conversion of cis to trans double bonds (Proell et al., 2002), lowering the fluidity of membranes and affecting their function. Oxidative attacks by superoxide and learn more other free radicals tend to break down unsaturated fatty acids, mainly PUFA (Mattson & Grundy, 1985; Trotschansky & Rubbo, 2008), which levels tend to decrease in structures continuously exposed to oxidizing environments. This is in part corrected by turnover of membranes in cells, and by interchange with lipoproteins in RBC (Cooper et al., 1975; Dise, Goodman & Rasmussen, 1980; Quarfordt & Hilderman, 1970; Reed, Murphy & Roberts, 1968). However, the marked lack of PUFA (and absence of ��-3) indicate that: (A) The postulated outer layer of lipid in RBC should be rather permanent, at least enough to show the effects of oxidation and nitration on its fatty acids. (B) This lipid is repeatedly exposed (for all its functional life) to highly oxidative microenvironments in capillary beds. (C) The lipid occupies BIBW2992 cell line a limited and defined space on the cells, which is not directly affected by the availability (or turnover) of lipids in plasma. In any case, there must be a certain degree of interchange of lipids between the RBC outer lipid layer and plasma lipids since its comparison with lipoprotein fatty acid patterns shows a considerable degree of similitude if PUFA are excluded. Labelled fatty acids are rapidly incorporated into RBC SWAP70 (Leyton, Drury & Crawford, 1987), and interchange or reposition of PUFA in the outer layer of RBC membranes has been previously described (Dise, Goodman & Rasmussen, 1980; Reed, Murphy & Roberts, 1968). Furthermore, diets high in PUFA decrease the stiffness of RBC membranes in metabolic syndrome (Katan et al., 1997; P?schl et al., 1999). Probably there is a direct relationship between these phenomena, and this can be a function, so far not defined, of the external lipid layer of RBC. We postulate that it may act as an intermediate step for repairs (or protection) of the RBC membrane, since in mammals most maintenance systems must be external to the RBC, because they lack nuclei, ribosomes and most of the cell turnover machinery. We expected, at least in the rats with overweight, that as a consequence of the cyclic exposure and close contact of RBC with endothelia there would be a marked increase in trans fatty acids (Alemany, 2012), a consequence of the higher production of nitric oxide and other oxidative and nitrating agents (Ghasemi, Zahediasl & Azizi, 2012). The levels of trans fatty acids we actually found were small, but could not be justified by the residual levels found in the diet (
