Lipid peroxidation, prostacyclin and thromboxane A₂in pigs depleted of vitamin E and selenium and supplemented with linseed oil

Abstract

In a 2 x 2 balanced factorial experiment the biochemical effects on pigs of two dietary factors were investigated. The first factor was a-tocopherol and Se supplementation and the second factor was supplementation with a-tocopherol-stripped linseed oil. In pigs fed on diets depleted of a-tocopherol and Se, increases in concentrations of markers of Lipid peroxidation (4hydroxynonenal and hexanal) were observed. However, skeletal myopathy was only observed in those pigs fed on diets depleted of atocopherol and Se and supplemented with oil. In those pigs, increased lipid peroxidation was observed in heart and supraspinatus muscle. The plasma concentration of thromboxane B, was increased in pigs fed on diets depleted of a-tocopherol and Se, suggesting an increased tendency towards platelet aggregation. However, this change was reversed in pigs depleted of a-tocopherol and Se, but supplemented with oil. This may have been a consequence of loss of arachidonic acid, the substrate for thromboxane formation, as a result of Lipid peroxidation.

Lipid and protein oxidation of α-linolenic acid-enriched pork during refrigerated storage as influenced by diet supplementation with olive leaves (Olea europea L.) or α-tocopheryl acetate

“…Table 3 also shows that the increase in n− 3 fatty acids was accompanied by a corresponding decrease (p ≤ 0.05) in arachidonic acid. This is consistent with other authors who reported a decrease in arachidonic acid in heart and supraspinatus muscles, but not in longissimus muscle when linseed oil was fed to pigs (Nolan, Kennedy, Blanchflower, & Kennedy, 1995). These authors suggested that this decrease was probably the result of peroxidation of arachidonic acid.…”

“…However, the extent of lipid oxidation differed (p≤0.05) between the dietary treatments, the increase being higher for the L group that had been dietary supplemented with 3% linseed oil, which is rich in α-linolenic acid. Group S that had been dietary supplemented with sunflower oil, which is rich in linoleic acid, presented MDA values lower (p≤0.05) than those of the L group at all time points, probably due to the fact that α-linolenic acid is more prone to oxidation than linoleic acid (Nolan et al, 1995). Τhe LOL5 group presented MDA values lower (p≤0.05) than those of the (S) group but higher (p≤0.05) than those of the LOL10 group, which in turn, presented MDA values higher (p≤0.05) than those of the LE group, at all storage times.…”

The effect of linseed diet on carcass value traits and fatty acid composition in muscle and fat tissue of fattening pigs

“…The desaturase and elongase activities seem to be more focused on the synthesis of n-3 instead of on the synthesis of n-6 fatty acids metabolites. On the contrary, Nolan et al (1995) did not report a decrease in arachidonic acid content in the longissimus muscle by feeding linseed oil. Sheard et al (2000) and Hoz et al (2003) studied the influence of linseed-rich test diet on fatty acid content in meat.…”

Assessment of requirements for selenium and adequacy of selenium status: a review

“…Combined selenium and vitamin E deficiency has also resulted in unfavourable lipid profiles in animal models (Mazur et al, 1996). A protective effect of selenium and vitamin E against lipid peroxidation has been observed and a possible mechanism of action through GPx or selenoprotein P has been proposed (Awad et al, 1994;Burk et al, 1995;Nolan et al, 1995). Results of the NPC trial (Clark et al, 1996) suggest an involvement of vitamin E, in that subjects ranking below the median plasma a-tocopherol concentration at entry to the study showed higher rates of subsequent carcinomas and greater apparent protective effects of selenium supplementation during the course of the trial ).…”