Dietary oxidised lipids,health consequences and novel food technologies that thwart food lipid oxidation: an update

Processed foods are popular and their consumption is expected to grow globally. Food processing and manufacturing promote lipid oxidation in foods rich in polyunsaturated fatty acids and cholesterol. This review focuses on how various food manufacturing/processing techniques promote lipid oxidation in grains, meats and meat products, dairy and fats/oils. This review also considers emerging evidence from animal and human studies that suggest a link between dietary oxidised lipid consumption and chronic disease risk. An update on novel food technologies that limit food lipid oxidation is discussed so as to inform both food scientists and dietitians/nutritionists to direct future efforts in not only continuing to bring these novel technologies to the market place but also conduct clinical trials to establish their role in human health.     

Effects of pharmacological amounts of S‐allylcysteine on lipids in normal and isoproterenol‐induced myocardial infarction in rats

The present study evaluates the effect of S‐allylcysteine on marker enzymes, serum and myocardial lipids in normal and isoproterenol‐induced myocardial infarction in male Wistar rats. A significant increase in the activities of marker enzymes such as creatine kinase, lactate dehydrogenase, aspartate transaminase and alanine transaminase in serum of isoproterenol (150 mg kg^?1)‐treated rats was observed. The levels of serum lipids (cholesterol, triglycerides, free fatty acids and phospholipids) were significantly increased, while the levels of myocardial cholesterol, triglycerides and free fatty acids were significantly increased in isoproterenol‐administered rats. The concentration of myocardial phospholipids was significantly decreased in isoproterenol‐administered rats. Oral pretreatment with S‐allylcysteine at doses of 50, 100 and 150 mg kg^?1 using an intragastric tube daily for a period of 45 days positively modulated the biochemical alterations caused by isoproterenol. The effect of S‐allylcysteine at a dose of 150 mg kg^?1 showed a better cardioprotective effect than the other two doses (50 and 100 mg kg^?1). α‐Tocopherol (60 mg kg^?1) administration orally using an intragastric tube to rats daily for 45 days also exhibited a significant cardioprotective effect. The effect of S‐allylcysteine was compared with α‐tocopherol. Oral administration of S‐allylcysteine (50, 100 and 150 mg kg^?1) to normal rats did not show any significant change in this study. Thus, from the present study it can be concluded that a pharmacological dose of S‐allylcysteine exerts a protective effect against isoproterenol‐induced myocardial infarction in rats. Copyright © 2006 Society of Chemical Industry     

Fatty acid composition of herring (Clupea harengus L.): influence of time and place of catch on n‐3 PUFA content

The fatty acid composition (FAC) was determined in muscle samples from 963 herring (Clupea harengus L.) caught during 2001–2003 in waters around Denmark. The overall variation in FAC was mainly related to seasonal (summer or winter) and annual (2001, 2002 or 2003) variation. No clear variation due to place of catch (Baltic Sea, Skagerrak, Kattegat or the northern, western or eastern part of the North Sea) was found. Of the nutritionally important n‐3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), EPA seemed to show a seasonal variation, with the highest amount during summer, whereas no periodic variation was observed for DHA. Herring from one catch, however, were found to have an extraordinarily high amount of EPA (11%) compared with all other catches (amounts of EPA ranging from 4 to 8%). This high EPA content found only in herring caught in May 2003 in the northern North Sea (NSN) was in large contrast to the herring caught in the same place 3 months earlier, which had the lowest EPA content overall. The abrupt increase in EPA level from February to May was not correlated with biological parameters such as spawning type, maturity status, age, sex and size, but it might be related to variation in the FAC of the calanoid copepods on which the herring feed. Considering the nutritional aspects, the high‐EPA herring from the NSN catch in May 2003 had a relatively low lipid content (7%), making them highly suitable for human consumption. Copyright © 2007 Society of Chemical Industry     

Effects of endogenous flour lipids on the quality of short‐dough biscuits

Fractionation and reconstitution techniques were used to study the contribution of endogenous flour lipids to the quality of short‐dough (shortcake type) biscuits. Biscuit flour was defatted with chloroform and baked with bakery fat, but without endogenous lipid. Short‐dough biscuits baked from defatted flour had smaller diameters, and were flatter, denser and harder than control biscuits. Defatted flour shortcake doughs exhibited different rheological behaviour from the control samples, showing higher storage and loss moduli (G′ and G″ values), ie higher viscoelasticity. Functionality was restored when total non‐starch flour lipids were added back to defatted flour. The polar lipid fraction had a positive effect in restoring flour quality whereas the non‐polar lipid fraction had no effect. Both fractions were needed for complete restoration of both biscuit quality and dough rheological characteristics. A study of the microstructure of defatted biscuits revealed that their gluten protein was more hydrated and developed than the gluten of the control biscuits. This conclusion was supported by the higher water absorption of the defatted gluten. Copyright © 2004 Society of Chemical Industry     

Possible abilities of dietary factors to prevent and treat diabetes via the stimulation of glucagon‐like peptide‐1 secretion

There is a pressing need for countermeasures against diabetes, which has increased in incidence, becoming a global issue. Glucagon‐like peptide‐1 (GLP‐1), a molecule secreted in enteroendocrine L cells in the lower small and large intestines, is thought to be one of the most important molecular targets for the prevention and treatment of diabetes. There has been increasing interest in the possible ability of dietary factors to treat diabetes via modulating GLP‐1 secretion. There is thought to be a close relationship between incretin and diet, and the purported best approach for using dietary factors to increase GLP‐1 activity is promotion of secretion of endogenous GLP‐1. It have been reported that nutrients as well as various non‐nutrient dietary factors can function as GLP‐1 secretogogues. Here, we present our findings on the GLP‐1 secretion‐stimulating functions of two dietary factors, curcumin and extract of edible sweet potato leaves, which contain caffeoylquinic acid derivatives. However, it is necessary to reveal in greater detail the stimulation of GLP‐1 secretion by dietary factors for preventing and treating diabetes. It is desirable to clarify the exact GLP‐1 secretory pathway, the effect of metabolites derived from dietary factors in gut lumen, and the relationship between incretin and meal.     

Naringenin up‐regulates the expression of death receptor 5 and enhances TRAIL‐induced apoptosis in human lung cancer A549 cells

Scope: While TRAIL is relatively non‐toxic to normal cells, it can selectively induce apoptosis in many types of transformed cells. Nevertheless, some non‐small cell lung cancer (NSCLC) cells are particularly resistant to the effects of TRAIL. Here, we report that in combination with naringenin exposure to TRAIL induced apoptosis in TRAIL‐resistant NSCLC A549 cells with no detectable inhibitory effects on cell proliferation of normal lung fibroblast cells. Methods and results: Cytotoxicity was evaluated by MTT assay. Apoptosis was detected using DAPI staining, and flow cytometry. The protein levels were determined by Western blot analysis. Caspase activity was measured using a colorimetric assay. For knockdown of Bid and DR5 expression, Bid and DR5 siRNAs were transfected into cells via lipofection. We could show that following exposure to naringenin, DR5 proteins were up‐regulated and knockdown of DR5 expression by siRNA attenuated naringenin plus TRAIL‐induced apoptosis. Naringenin and TRAIL effectively induced Bid cleavage and siRNA‐mediated silencing of Bid reduced the sensitizing effect of naringenin. Furthermore, co‐treatment with naringenin and TRAIL resulted in reduction of the clonogenic capacity of A549 cells, and surviving clones could be re‐sensitized for repeated TRAIL treatment. Conclusion: Our results indicate that treatment with a combination of TRAIL and naringenin may be a safe strategy for treatment of resistant NSCLC.     

Methionine restriction up‐regulates the expression of the pi class of glutathione S‐transferase partially via the extracellular signal‐regulated kinase‐activator protein‐1 signaling pathway initiated by glutathione depletion

Understanding the molecular events underlying gene regulation by amino acids has attracted increasing attention. Here, we explored whether the mechanism by which methionine restriction affects the expression of the π class of glutathione S‐transferase (GSTP) is related to oxidative stress initiated by glutathione (GSH) depletion. Rat primary hepatocytes were cultured in an L‐15‐based medium in the absence or presence of 200 μM L ‐buthionine sulfoximine (BSO) or in a methionine‐restricted L‐15 medium supplemented with 20 μM L ‐methionine up to 72 h. BSO and methionine restriction time‐dependently induced GSTP mRNA and protein expression in a similar pattern accompanied by a decrease in the cellular GSH level. The phosphorylation of extracellular signal‐regulated kinase (ERK), but not of c‐Jun NH₂‐terminal kinase and p38, was stimulated by methionine restriction and BSO. Electromobility gel shift assay showed that the DNA‐binding activity of nuclear activator protein‐1 (AP‐1) increased in cells exposed to methionine restriction or BSO. With the ERK inhibitor FR180204, AP‐1 activation and GSTP expression were abolished. Moreover, the induction of GSTP by methionine restriction and BSO was reversed by GSH monoethyl ester and N‐acetylcysteine. Our results suggest that methionine restriction up‐regulates GSTP gene expression, which appears to be initiated by the ERK‐AP‐1 signaling pathway through GSH depletion in rat hepatocytes.