Consumers demand both safer and more nutritious food products exempt of non-natural origin preservatives or other food additives. In this frame, products with lower fat content and/or a higher ratio in unsaturated fatty acids, especially n-3 fatty acids, are desired because these lipids can help prevent the development of cardiovascular and inflammatory pathologies. The intake of meat products is of interest because they are an excellent source of vitamins and minerals. In addition, the shelf-life of meat products can be extended by the presence of natural antioxidants coming from different sources such as plant extracts. Therefore, different strategies have been studied to improve the nutritional value, oxidative stability, and sensory characteristics of meat products and eggs through different mineral and natural dietary supplements. In comparison to other strategies, dietary supplements present the advantage that first the living animals may efficiently distribute the compounds throughout the tissues and second, the dietary supplementation is safer because the resulting enriched meat products and eggs ensure tolerable amounts in humans. Poultry meats and eggs are widely consumed and their fatty acid profile and tocopherol content can be easily modified through different dietary strategies thus being excellent models to improve their nutritional value and oxidative stability.

A factorial design was used to study the effect of dietary fish oil (1.25% and 2.5%), all-rac-α-tocopheryl acetate (70 and 140 mg/kg), and Zn supplementation (0 and 200 mg/kg) on the composition and consumer acceptability of chicken meat stored at -20°C for 5 mo. Supplementation of the diet with all-rac-α-tocopheryl acetate increased the α-tocopherol content in meat. The fatty acid composition of the meat was affected only by the amount of fish oil. Diets supplied with 2.5% fish oil produced meat with an eicosapentaenoic and docosahexaenoic acid content double that of diets supplied with 1.25% fish oil. Zn supplementation did not affect the content of this mineral in the meat. Moreover, the consumer acceptability of meat samples showed no significant differences between dietary treatments after 5 mo of storage at -20°C or with respect to a freshly cooked commercial sample used as a blind control.

The contribution of metabolic factors to the severity of liver disease is not completely understood. In this study, apolipoprotein E-deficient (ApoE^−/−) mice were evaluated to define potential effects of hypercholesterolemia on the severity of carbon tetrachloride (CCl₄)-induced liver injury. Under baseline conditions, hypercholesterolemic ApoE^−/− mice showed increased hepatic oxidative stress (SOD activity/4-hydroxy-2-nonenal immunostaining) and higher hepatic TGF-β₁, MCP-1, and TIMP-1 expression than wild-type control mice. After CCl₄ challenge, ApoE^−/− mice exhibited exacerbated steatosis (Oil Red O staining), necroinflammation (hematoxylin-eosin staining), macrophage infiltration (F4/80 immunohistochemistry), and fibrosis (Sirius red staining and α-smooth muscle actin immunohistochemistry) and more severe liver injury [alanine aminotransferase (ALT) and aspartate aminotransferase] than wild-type controls. Direct correlations were identified between serum cholesterol and hepatic steatosis, fibrosis, and ALT levels. These changes did not reflect the usual progression of the disease in ApoE^−/− mice, since exacerbated liver injury was not present in untreated age-paired ApoE^−/− mice. Moreover, hepatic cytochrome P-450 expression was unchanged in ApoE^−/− mice. To explore potential mechanisms, cell types relevant to liver pathophysiology were exposed to selected cholesterol-oxidized products. Incubation of hepatocytes with a mixture of oxysterols representative of those detected by GC-MS in livers from ApoE^−/− mice resulted in a concentration-dependent increase in total lipoperoxides and SOD activity. In hepatic stellate cells, oxysterols increased IL-8 secretion through a NF-κB-independent mechanism and upregulated TIMP-1 expression. In macrophages, oxysterols increased TGF-β₁ secretion and MCP-1 expression in a concentration-dependent manner. Oxysterols did not compromise cell viability. Taken together, these findings demonstrate that hypercholesterolemic mice are sensitized to liver injury and that cholesterol-derived products (i.e., oxysterols) are able to induce proinflammatory and profibrogenic mechanisms in liver cells.