In the present study, the protective role of purified C-phycoerythrin (C-PE) against diabetic complications and Cu-mediated lipoprotein oxidation was evaluated. C-PE (25 and 50 mg/kg body weight per d) was administered to experimental streptozotocin–nicotinamide-induced type 2 diabetic male rats for 28 d. C-PE treatment successfully ameliorated diabetic complications by decreasing food intake, organ weights, serum concentrations of glucose, cholesterol, TAG, VLDL-cholesterol, creatinine, uric acid and thiobarbituric acid-reactive substances (TBARS), with increases in body weight, Hb, total protein, bilirubin and ferric-reducing ability of plasma values. Hepatic and renal tissues demonstrated significant decreases in TBARS, lipid hydroperoxide and conjugated diene contents, with increases in superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione, vitamin E and vitamin C levels. Furthermore, the 4-week ex vivo and in vitro administration of C-PE (0·5 and 1·0 mg/ml) indicated a decrease in Cu-mediated serum oxidation. The kinetics of the LDL oxidation profile showed significant prolongation of the lag phase with declines in oxidation rate, conjugated dienes, lipid hydroperoxide and TBARS. Results indicated the involvement of C-PE in the amelioration of diabetic complications by significant reductions in oxidative stress and oxidised LDL-triggered atherogenesis.

During atherogenesis, a pathological accumulation of lipids occurs within aortic intimal macrophages through uptake of plasma oxidised LDL (oxLDL). The aim of the present study was to determine whether macrophage uptake of plasma oxLDL and LDL susceptibility to oxidation may be determined by quantity and quality of dietary fat. Twenty healthy young men were subjected to three dietary periods, each lasting 4 weeks. The first was an SFA-enriched diet (38 % fat, 20 % SFA), which was followed by a carbohydrate (CHO)-rich diet (30 % fat, < 10 % SFA, 55 % CHO) or a MUFA olive oil-rich diet (38 % fat, 22 % MUFA) following a randomised cross-over design. After each diet period, LDL particles were oxidised with Cu ions to determine LDL susceptibility to oxidation and subsequently incubated with the U937-macrophage cell line to determine the percentage of uptake of plasma oxLDL. The shift from the MUFA diet to the SFA- or CHO-rich diets reduced the resistance of LDL particles to oxidation, decreasing lag time (P = 0·038) and increasing the propagation rate (P = 0·001). Furthermore, the MUFA-rich diet demonstrated reduced macrophage uptake of plasma oxLDL (P = 0·031) as compared with the SFA-rich diet. Finally, macrophage uptake of plasma oxLDL was correlated (r 0·45; P = 0·040) with total amount of conjugated dienes after LDL oxidation. Our data suggest that a MUFA-rich diet may have favourable effects on cardiovascular risk since it prevents the oxidative modifications of LDL and reduces macrophage uptake of plasma oxLDL.

Fish-oil supplementation can reduce circulating triacylglycerol (TG) levels and cardiovascular risk. This study aimed to assess independent associations between changes in platelet eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and fasting and postprandial (PP) lipoprotein concentrations and LDL oxidation status, following fish-oil intervention. Fifty-five mildly hypertriacylglycerolaemic (TG 1·5–4·0 mmol/l) men completed a double-blind placebo controlled cross over study, where individuals consumed 6 g fish oil (3 g EPA+DHA) or 6 g olive oil (placebo)/d for two 6-week intervention periods, with a 12-week wash-out period in between. Fish-oil intervention resulted in a significant increase in the platelet phospholipid EPA (+491 %, P<0·001) and DHA (+44 %, P<0·001) content and a significant decrease in the arachidonic acid (-10 %, P<0·001) and γ-linolenic acid (-24 %, P<0·001) levels. A 30 % increase in ex vivo LDL oxidation (P<0·001) was observed. In addition, fish oil resulted in a significant decrease in fasting and PP TG levels (P<0·001), PP non-esterified fatty acid (NEFA) levels, and in the percentage LDL as LDL-3 (P=0·040), and an increase in LDL-cholesterol (P=0·027). In multivariate analysis, changes in platelet phospholipid DHA emerged as being independently associated with the rise in LDL-cholesterol, accounting for 16 % of the variability in this outcome measure (P=0·030). In contrast, increases in platelet EPA were independently associated with the reductions in fasting (P=0·046) and PP TG (P=0·023), and PP NEFA (P=0·015), explaining 15–20 % and 25 % of the variability in response respectively. Increases in platelet EPA+DHA were independently and positively associated with the increase in LDL oxidation (P=0·011). EPA and DHA may have differential effects on plasma lipids in mildly hypertriacylglycerolaemic men.