Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure to particulate emissions from printer and cigarette smoke affects the structure and function of mitochondria, which may account for the pathogenesis of respiratory diseases. The addition of charge for the pollutant aerosols may increase the toxicity by their deposition in the lower respiratory tract. The mitochondrial damage in the lung of asthmatic mice was assessed by examining the levels of reactive oxygen species (ROS), lipid peroxides, reduced glutathione, and the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, complexes I to IV, and cytochrome c. The oxidative phosphorylation (levels of adenosine triphosphatase) was evaluated for the assessment of mitochondrial functional capacity. We found highly significant elevated levels of ROS, lipid peroxides, and decreased levels of mitochondrial enzymes in the mice exposed to environmental tobacco smoke and printer emissions + environmental tobacco smoke (ETS). However, mice exposed to printer emissions alone exhibited slight significant variations in the parameters studied. From the results, we conclude that printer emissions exert a synergistic effect in the presence of ETS and induce intense damage to the lung mitochondria by disrupting the structural and functional integrity of the mitochondrial membrane.
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PMID:Oxidative stress and antioxidant defenses in asthmatic murine model exposed to printer emissions and environmental tobacco smoke. 2010 29

Larch bark procyanidins (LBPCs) have not only antioxidant and antitumor properties, but also strong bacteriostatic effects. However, it is not clear about the antibacterial mechanisms of LBPC. In this work, the antibacterial effects and mechanisms of LBPC on Staphylococcus aureus were studied in the aspects of morphological structure, cell wall and membrane, essential proteins, and genetic material. The results showed that LBPC effectively inhibited bacterial growth at a minimum inhibitory concentration of 1.75 mg/ml. Bacterial morphology was significantly altered by LBPC treatment, with the cell walls and membranes being destroyed. Extracellular alkaline phosphatase content, bacterial fluid conductivity, and Na+/K+-ATPase and Ca2+-ATPase activities in the membrane system were all increased. In the energy metabolic systems, the activities of succinate dehydrogenase, malate dehydrogenase, and adenosine triphosphatase (ATPase) were all decreased, resulting in a slowdown of metabolism and bacterial growth inhibition. Changes of protein content and composition in the bacteria suggested that the protein expression system was affected. In addition, LBPC was found to bind to DNA grooves to form complexes. Thus, LBPC has a very strong inhibitory effect on S. aureus and can kill S. aureus by destroying the integrity and permeability of the cell wall and cell membrane, affecting protein synthesis, and binding to DNA.
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PMID:Antimicrobial activity and mechanism of Larch bark procyanidins against Staphylococcus aureus. 2909 73


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