Synthetic antioxidants are widely used in the food industry. However, the potential toxicity, carcinogenic effects, and possible health damage caused by the ingestion of synthetic compounds, and also consumer concern about the safety of such additives has motivated the food industry to search for natural alternatives. Natural compounds with antioxidant properties are able to retard or prevent lipid oxidation in food. Animal sources like fish, eggs, meats, and dairy products are essential foods for human health due to their lipid fraction with high contents of unsaturated compounds, such as polyunsaturated fatty acids and cholesterol. However, these unsaturated lipids when exposed to favorable factors can become oxidized, which leads to sensory and nutritional losses as well as the formation of oxidized compounds known as cholesterol oxidation products or COPs. COPs are associated with deleterious health effects, such as inflammation, cytotoxicity, atherogenesis, carcinogenesis, and alterations in cell membrane properties, as well as the development of degenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and other chronic diseases. Thus, the use of natural antioxidants can be an alternative to synthetics to prevent the formation of COPs and extend the shelf life of foods susceptible to oxidative deterioration. This review brings together information concerning the use of natural antioxidants as a strategy to control cholesterol oxidation.

Studies have shown autophagy participation in the immunopathology of inflammatory diseases. However, autophagy role in asthma and in eosinophil extracellular traps (EETs) release is poorly understood. Here, we attempted to investigate the autophagy involvement in EETs release and in lung inflammation in an experimental asthma model. Mice were sensitized with ovalbumin (OVA), followed by OVA challenge.Before the challenge with OVA, mice were treated with an autophagy inhibitor, 3-methyladenine (3-MA). We showed that 3-MA treatment decreases the number of eosinophils, eosinophil peroxidase (EPO) activity, goblet cells hyperplasia, proinflammatory cytokines, and nuclear factor kappa B (NFκB) p65 immunocontent in the lung. Moreover, 3-MA was able to improve oxidative stress, mitochondrial energy metabolism, and Na + , K + -ATPase activity. We demonstrated that treatment with autophagy inhibitor 3-MA reduced EETs formation in the airway. On the basis of our results, 3-MA treatment can be an interesting alternative for reducing lung inflammation, oxidative stress, mitochondrial damage, and EETs formation in asthma. K E Y W O R D Sasthma, autophagy, eosinophil extracellular traps, eosinophils, inflammation

In asthma, there are high levels of inflammatory mediators, reactive oxygen species (ROS), and eosinophil extracellular traps (EETs) formation in airway. Here, we attempted to investigate the ROS involvement in EETs release and airway inflammation in OVA-challenged mice. Before the intranasal challenge with ovalbumin (OVA), animals were treated with two ROS inhibitors, N-acetylcysteine (NAC) or diphenyleneiodonium (DPI). We showed that NAC treatment reduced inflammatory cells in lung. DPI and NAC treatments reduced eosinophil peroxidase (EPO), goblet cells hyperplasia, proinflammatory cytokines, NFκB p65 immunocontent, and oxidative stress in lung. However, only the NAC treatment improved mitochondrial energy metabolism. Moreover, the treatments with DPI and NAC reduced EETs release in airway. This is the first study to show that ROS are needed for EETs formation in asthma. Based on our results, NAC and DPI treatments can be an interesting alternative for reducing airway inflammation, mitochondrial damage, and EETs release in asthma. K E Y W O R D S diphenyleneiodonium, DNA extracellular traps, experimental asthma, N-acetylcysteine, oxidative stress

The endothelial-to-mesenchymal transition (EndMT) is a biological process where endothelial cells (ECs) acquire a fibroblastic phenotype after concomitant loss of the apical-basal polarity and intercellular junction proteins. This process is critical to embryonic development and is involved in diseases such as fibrosis and tumor progression. The signaling pathway of the transforming growth factor β (TGF-β) is an important molecular route responsible for EndMT activation. However, it is unclear whether the anatomic location of endothelial cells influences the activation of molecular pathways responsible for EndMT induction. Our study investigated the molecular mechanisms and signaling pathways involved in EndMT induced by TGF-β2 in macrovascular ECs obtained from different sources. For this purpose, we used four types of endothelial cells (coronary artery endothelial cells, CAECs; primary aortic endothelial cells PAECs; human umbilical vein endothelia cells, HUVECs; and human pulmonary artery endothelial cells, HPAECs) and stimulated with 10 ng/mL of TGF-β2. We observed that among the ECs analyzed in this study, PAECs showed the best response to the TGF-β2 treatment, displaying phenotypic changes such as loss of endothelial marker and acquisition of mesenchymal markers, which are consistent with the EndMT activation. Moreover, the PAECs phenotypic transition was probably triggered by the extracellular signal–regulated kinases 1/2 (ERK1/2) signaling pathway activation. Therefore, the anatomical origin of ECs influences their ability to undergo EndMT and the selective inhibition of the ERK pathway may suppress or reverse the progression of diseases caused or aggravated by the involvement EndMT activation.

Fish and fish products are important from a nutritional point of view due to the presence of high biological value proteins and the high content of polyunsaturated fatty acids, especially those of the n-3 series, and above all eicosapentaenoic acid and docosahexaenoic acid. However, these important food products also contain significant amounts of cholesterol. Although cholesterol participates in essential functions in the human body, it is unstable, especially in the presence of light, oxygen, radiation, and high temperatures that can cause the formation of cholesterol oxidation products or cholesterol oxides, which are prejudicial to human health. Fish processing involves high and low temperatures, as well as other methods for microbiological control, which increases shelf life and consequently added value; however, such processes favor the formation of cholesterol oxidation products. This review brings together data on the formation of cholesterol oxides during the preparation and processing of fish into food products which are recognized and recommended for their nutritional properties.