Deep-fried vegetable oils are reused multiple times to save costs, and their chronic consumption may cause organ dysfunction. In this study, we assessed the modulatory effects of lipid-solubles from ginger and turmeric that may migrate to oils during heating, on the cardio-hepatic antioxidant defence response and blood pressure in rats. Male Wistar rats were fed with: (1) control (native rapeseed (N-CNO) or native sunflower (N-SFO)) oil, (2) heated (heated rapeseed (H-CNO) or heated sunflower (H-SFO)) oil and (3) heated oil with ginger or turmeric (heated rapeseed oil with ginger (H-CNO + GI) or heated rapeseed oil with turmeric (H-CNO + TU), heated sunflower oil with ginger (H-SFO + GI) or heated sunflower oil with turmeric (H-SFO + TU)) for 120 d. Oxidative stress (OS) markers, antioxidant enzymes, nitric oxide synthase-2 (NOS-2), intercellular adhesion molecule-1 (ICAM-1), nuclear factor erythroid 2-related factor 2 (NRF-2), markers of hepatic and cardiac function and blood pressure were assessed. Feeding heated oils (H-CNO or H-SFO) (1) increased OS markers, NOS-2 and ICAM-1 expression; (2) decreased antioxidant enzyme activity and NRF-2 level; (3) increased marker enzymes of hepatic and cardiac function and (4) increased systolic and diastolic blood pressure significantly (P < 0·05), when compared with respective native oils (N-CNO or N-SFO). However, feeding oils heated with ginger or turmeric positively countered the changes induced by heated oils. Consumption of repeatedly heated oil causes cardio-hepatic dysfunction by inducing OS through NRF-2 down-regulation. Lipid-solubles from ginger and turmeric that may migrate to oil during heating prevent the oxidative stress and blood pressure triggered by heated oils in rats.

The effects of the addition of heated oils to feeds (3%, w/w) and the dietary supplementation with α-tocopheryl acetate (TA; 100 mg/kg) and Zn (200 mg/kg) on rabbit tissue fatty acid (FA) composition and on the Zn, Cu, Fe and Se content in meat were assessed. Heating unrefined sunflower oil (SO) at 55°C for 245 h increased its content in primary oxidation products and reduced its α-tocopherol content. However, this did not significantly affect tissue FA composition. Heating SO at 140°C for 31 h increased its content in secondary oxidation products and in some FA isomers as c9,t11-CLA and di-trans CLA. This led to increases in di-trans CLA in liver and in t9,c12-18:2 in meat. The c9,t11-CLA was the most incorporated CLA isomer in tissues. The dietary supplementation with α-TA did not affect the FA composition of plasma, liver or meat. The cooking of vacuum-packed rabbit meat at 78°C for 5 min reduced significantly but slightly its polyunsaturated FA content. The dietary supplementation with Zn did not modify the content of Zn, Fe or Se in meat, but it reduced its Cu content. On the other hand, it increased the content of some FAs in meat when SO heated at 140°C for 31 h was added to feeds.

The effect of heated sunflower oil consumption on α-tocopherol status, fatty acid composition and oxidative stability of chicken tissues was investigated. Chicks were fed on diets containing (g/kg): fresh sunflower oil (FSO) 40, heated sunflower oil (HSO) 40 or heated sunflower oil (40) supplemented with α-tocopheryl acetate (HSE) to a similar α-tocopherol concentration as the FSO diet. Concentrations of α-tocopherol in tissues of chicks fed on HSO and HSE were significantly lower than those of chicks fed on FSO. Significant correlations were observed between plasma α-tocopherol concentration and the α-tocopherol concentrations of other tissues (r < 0·67, P < 0·005) and between log plasma α-tocopherol and plasma thiobarbituric acid-reacting substances (TBARS) concentrations (r – 0·851, P < 0·001). The concentrations of TEARS in tissues of chicks fed on the various diets were generally very similar before stimulation of peroxidation with Fe–ascorbate. Susceptibility of tissues to Fe–ascorbate-induced lipid peroxidation was increased by feeding HSO. Supplementation with α-tocopheryl acetate reduced susceptibility tc lipid oxidation to varying degrees, depending on the tissue. The results suggest that chronic ingesrion of oxidized lipids may compromise free-radical-scavenging activity in vivo by depleting α-tocopherol in the gastrointestinal tract, or possibly in plasma and other tissues.