Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.6.3.1 (NADPH oxidase)
11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cumulative doses of doxorubicin, a potent anticancer drug, lead to serious myocardial dysfunction. Numerous mechanisms including apoptosis have been proposed to account for its cardiotoxicity. Cardiac apoptosis induced by doxorubicin has been related to excessive reactive oxygen species production by the mitochondrial NADH dehydrogenase. Here, we explored whether doxorubicin treatment activates other superoxide anion generating systems such as the NADPH oxidases, membrane-embedded flavin-containing enzymes, and whether the subsequent oxidative stress contributes to apoptosis. We showed that doxorubicin treatment of rat cardiomyoblasts H9c2 triggers increases in caspase-3 like activity and hypoploid cells, both common features of apoptosis. Doxorubicin exposure also leads to a rapid superoxide production through NADPH oxidase activation. Inhibition of these enzymes using diphenyliodonium and apocynin reduces doxorubicin-induced reactive oxygen species production, caspase-3 like activity and sub-G1 cell population. In conclusion, NADPH oxidases participate to doxorubicin-induced cardiac apoptosis.
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PMID:NADPH oxidases participate to doxorubicin-induced cardiac myocyte apoptosis. 1969 79

Increased oxidative stress and apoptosis were detected in atherosclerotic lesions. Oxidized low-density lipoprotein (oLDL) may induce oxidative stress and apoptosis via multiple pathways in vascular endothelial cells (EC). Delphinidin-3-glucoside (D3G), an anthocyanidin glycan enriched in dark-skin berries, may neutralize those effects of oLDL in EC. The present study demonstrated that oLDL increased the generation of intracellular NADPH-dependent superoxide and impaired redox status in cultured porcine aortic EC (PAEC). The activities of mitochondrial respiratory chain complex I-IV and the contents of NADH dehydrogenase (ND)1, ND6 (complex I enzyme subunits), or cytochrome b (complex III enzyme subunit) were significantly reduced in PAEC treated with oLDL compared to controls. Treatment with oLDL significantly increased the abundances of NADPH oxidase (NOX)2, NOX4, and p22phox in PAEC. oLDL reduced cell viability and the protein content of B-cell lymphoma (Bcl)-2, but increased the content of caspase 3 in PAEC. Co-treatment with D3G prevented oLDL-induced increases in intracellular superoxide or in the protein content of NOX2, NOX4, p22phox, or caspase 3, inhibited the impairment of redox statues or cell viability, and prevented the attenuation of mitochondrial enzyme activities and the reductions of Bcl-2, ND1, or cytochrome b contents in PAEC. The findings suggest that oLDL induced oxidative stress and apoptosis in EC, which was associated with the activation of NOX, the impairment of mitochondrial respiration chain enzymes, and the disorder of key regulators for apoptosis. D3G neutralized the harmful effects of oLDL on oxidative stress, mitochondrial dysfunction, and apoptosis in cultured vascular EC.
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PMID:Influence of delphinidin-3-glucoside on oxidized low-density lipoprotein-induced oxidative stress and apoptosis in cultured endothelial cells. 2227 27

The respiratory chain of Corynebacterium glutamicum was investigated, especially with respect to a cyanide-resistant respiratory chain bypass oxidase. The membranes of C. glutamicum had NADH, succinate, lactate, and NADPH oxidase activities, and menaquinone, and cytochromes a 598, b 562(558), and c 550 as respiratory components. The NADH, succinate, lactate, and NADPH oxidase systems, all of which were more cyanide-resistant than N,N,N',N'-tetramethyl-p-phenylene diamine oxidase activity (cytochrome aa 3 terminal oxidase), had different sensitivities to cyanide; the cyanide sensitivity of these oxidase systems increased in the order, NADPH, lactate, NADH, and succinate. Taken together with the analysis of redox kinetics in the cytochromes and the effects of respiratory inhibitors, the results suggested that there is a cyanide-resistant bypass oxidase branching at the menaquinone site, besides cyanide-sensitive cytochrome oxidase in the respiratory chain. H(+)/O measurements with resting cells suggested that the cyanide-sensitive respiratory chain has two or three coupling sites, of which one is in NADH dehydrogenase and the others between menaquinone and cytochrome oxidase, but the cyanide-resistant bypass oxidase may not have any proton coupling site. NADPH and lactate oxidase systems were more resistant to UV irradiation than other systems and the UV insensitivity was highest in the NADPH oxidase system, suggesting that a specific quinone resistant to UV or no such a quinone works in at least NADPH oxidase system while the UV-sensitive menaquinone pool does in other oxidase systems. Furthermore, superoxide was generated in well-washed membranes, most strongly in the NADPH oxidase system. Thus, it was suggested that the cyanide-resistant bypass oxidase system of C. glutamicum is related to the NADPH oxidase system, which may be involved in generation of superoxide anions and probably functions together with superoxide dismutase and catalase.
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PMID:NADPH Oxidase System as a Superoxide-generating Cyanide-Resistant Pathway in the Respiratory Chain of Corynebacterium glutamicum. 2738 51

To achieve the accumulation of targeted secondary metabolites, microorganisms must adopt various protection mechanisms to avoid or reduce damage to cells caused by abiotic stresses, which formed from the changes of physical and chemical culture conditions. The protection mechanism of Monascus sp. to tolerate high-concentration ammonium chloride was analyzed by sequential window acquisition of all theoretical mass spectra-mass spectrometry proteomics in this work, and the results indicated that abiotic stresses caused by high-concentration ammonium chloride inhibited the synthesis of chitin and glycoprotein, leading to a decrease in cell wall integrity and, thus, affecting cell growth. At the same time, it also inhibited the complex enzyme III and IV activities of the mitochondrial cytochrome respiratory chain, leading to an increase in reactive oxygen species (ROS) levels. With the aim to respond to abiotic stresses, the cross-protection mechanism was implemented in Monascus, including self-protection of the Monascus cell by promoting synthesis of trehalose, a molecular chaperone that facilitates protein folding (such as heat-shock protein) and autophagy-related proteins, through not the enzyme protection system (superoxide dismutase, peroxidase, catalase, NADPH oxidase, and alternative oxidase) but the glutathione/glutaredoxin system, to maintain the intracellular redox state and then eliminate or reduce ROS damage to the cell. At the same time, an alternative respiratory pathway related to NADH dehydrogenase was activated to balance the material and energy metabolism.
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PMID:Quantitative Proteomics Analysis by Sequential Window Acquisition of All Theoretical Mass Spectra-Mass Spectrometry Reveals a Cross-Protection Mechanism for Monascus To Tolerate High-Concentration Ammonium Chloride. 3248 1


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