Anti-TNF monoclonal antibody

Inflammation is an essential biological process for maintaining homeostasis in the body. However, excessive inflammatory response is closely related to many chronic diseases. Ammonia is a known environmental pollutant and a main harmful gas in the environment of livestock house. It causes deterioration of air quality and poses a threat to human and animal health. Chickens are very sensitive to ammonia. In order to assess the toxicity of ammonia to the heart, the pathology, ATPase activities, markers of oxidative stress, inflammatory pathways and inflammation markers were investigated in the hearts of chickens exposed to ammonia. The results showed that the cardiac pathological structure, oxidative stress index, and ATPase activity changed significantly in ammonia-treated chickens. In addition, the inflammation pathways (JAK/STAT and MAPK) were activated in the ammonia group, and the inflammatory markers (COX-2, TNF-alpha, NF-kappa B and PPAR-gamma) were significantly altered at both mRNA and protein levels. In conclusion, excess ammonia can activate inflammatory pathways through oxidative stress and abnormal energy metabolism, and induce cardiac inflammatory injury. Our findings will provide a new insight for better assessing the toxicity mechanism of ammonia on the heart. (C) 2020 Elsevier B.V. All rights reserved.

Exposure to ambient air particulate matter (PM) is associated with increased cardiorespiratory morbidity and mortality. In this context, alveolar macrophages exhibit proinflammatory and oxidative responses as a result of the clearance of particles, thus contributing to lung injury. However, the mechanisms linking these pathways are not completely clarified. Therefore, the oxinflammation phenomenon was studied in RAW 264.7 macrophages exposed to Residual Oil Fly Ash (ROFA), a PM surrogate rich in transition metals. While cell viability was not compromised under the experimental conditions, a proinflammatory phenotype was observed in cells incubated with ROFA 100 mu g/mL, characterized by increased levels of TNF-alpha and NO production, together with PM uptake. This inflammatory response seems to precede alterations in redox metabolism, characterized by augmented levels of H2O2, diminished GSH/GSSG ratio, and increased SOD activity. This scenario resulted in increased oxidative damage to phospholipids. Moreover, alterations in mitochondrial respiration were observed following ROFA incubation, such as diminished coupling efficiency and spare respiratory capacity, together with augmented proton leak. These findings were accompanied by a decrease in mitochondrial membrane potential. Finally, NADPH oxidase (NOX) and mitochondria were identified as the main sources of superoxide anion (O-2(center dot-)) in our model. These results indicate that PM exposure induces direct activation of macrophages, leading to inflammation and increased reactive oxygen species production through NOX and mitochondria, which impairs antioxidant defense and may cause mitochondrial dysfunction.