ABSTRACT
Rotenone is a specific inhibitor of the NADH dehydrogenase complex. In mitochondria, rotenone inhibitsthe oxidation of NADH to NAD, thereby blocking the oxidation of NAD and the substrates such asglutamate, alpha-ketoglutarate, and pyruvate. Rotenone also inhibits the mitochondrial respiratory chainbetween diphosphopyridine nucleotide and flavine.2, 4-Dinitrophenol – (DNP) is lipophilic weak acids that pick up a proton, transport across the mitochondrialinner membrane into the matrix, deprotonate, then exit as anions before repeating the catalytic cycle,and dissipating the proton gradient. In this situation, electrons continue to pass through the electrontransport system, reduce oxygen to water and metabolic rate, heat are increased, but ATP is lesssynthesized in this process.The macrolide antibiotic - oligomycin binds to the surface of the c8-10 ring of the Fo domain of ATPsynthase, making contact with two neighboring molecules and blocking proton flow, which explains theinhibitory effect on ATP synthesis. Intraperitoneal injection of oligomycin into the rat (0.5 mg per kg)reduces the oxygen consumption by about 50%; decreases ATP production by the aerobic pathway andincreases formation of lactate in blood serum. These changes may cause a decelerated metabolism andan increased formation of free radicals or ROS in membranes.
ABSTRACT
Background. This study is to determine mode of metabolism on triple collaboration bridges of traditional medicine, modern medicine and NCM.Goal. To determine membrane redoxy potentials three line involves important regulation factors on mode of metabolism which relationship connected with rlung, mkris, and badgan symbolic code.Materials and Methods. Only 81 healthy individuals were involved in the study. Proton leak was determined by quantity rate of MDA in cell membrane and membrane resistance, proton conductance was determined by serum and urine oxidase activity.Results. The table 1 shows quantity rate of membrane resistance was decreased 1.08-1.52 fold, HDL content was decreased, and however LDL was increased. This result is to manifest low proton leak which means this type is likely belonged to badgan symbolic code with qualities cold fatty, earth, water. The table 2 shows serum and urine oxidize activity 2.22-6.1 fold was increased, HDL content was increased; UCP-3 gene activity relatively was increased. This result is to manifest highproton conductance which means this type is likely belonged to mkris symbolic code with qualities hot fatty, fire.Conclusions:1. Individuals with high proton leak and slow proton conductance had serum and urine oxidize activity were weak, therefore there are visceral and subcutaneous fat were low.2. Individuals with medium proton leak and high proton conductance had serum and urine oxidize activity were high, therefore there are visceral was low and subcutaneous fat was high.3. Individuals with weak proton leak and medium proton conductance had serum and urine oxidize activity were medium, therefore there are visceral was high and subcutaneous fat was low.
ABSTRACT
The pathogenesis of chronic obstructive pulmonary disease (COPD) encompasses a number of injurious processes, including an abnormal inflammatory response in the lungs to inhaled particles and gases. Other processes, such as failure to resolve inflammation, abnormal cell repair, apoptosis, abnormal cellular maintenance programs, extracellular matrix destruction (protease/antiprotease imbalance), and oxidative stress (oxidant/antioxidant imbalance) also have a role. The inflammatory responses to the inhalation of active and passive tobacco smoke and urban and rural air pollution are modified by genetic and epigenetic factors. The subsequent chronic inflammatory responses lead to mucus hypersecretion, airway remodeling, and alveolar destruction. This article provides an update on the cellular and molecular mechanisms of these processes in the pathogenesis of COPD. During the past decade a plethora of studies have unravelled the multiple roles of nitric oxide (NO) in airway physiology and pathophysiology. In the respiratory tract, NO is produced by a wide variety of cell types and is generated via oxidation ofL-arginine that is catalyzed by the enzyme NO synthase (NOS). NOS exist in three distinct are forms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO derived from the constitutive are forms of NOS (nNOS and eNOS) and other NO-adduct molecules (nitrosothiols) have been shown to be modulators of bronchomotor tone. On the other hand, NO derived from iNOS seems to be a proinflammatory mediator with immunomodulatory effects. Finally, the production of NO under oxidative stress conditions secondarily generates strong oxidizing agents (reactive nitrogen species) that may modulate the development of chronic inflammatory airway diseases and/or amplify the inflammatory response.