Oxidase System (oxidase + system)

Distribution by Scientific Domains


Selected Abstracts


Biosensors Based on Aligned Carbon Nanotubes Coated with Inherently Conducting Polymers

ELECTROANALYSIS, Issue 13 2003
Mei Gao
Abstract The use of multiwalled aligned carbon nanotubes provides a novel electrode platform for inherently conducting polymer based biosensors. The example used here to highlight the usefulness of such a platform is the polypyrrole based glucose oxidase system for detection of glucose. The use of these three dimensional electrodes offers advantages in that large accessible enzyme loadings can be obtained within an ultrathin layer. It has also been found that the detection of H2O2 at these new electrode structures containing iron loaded nanotube tips can be achieved at low anodic potentials. The result is a sensitive and selective glucose sensor. [source]


Evidence for redox cycling of lawsone (2-hydroxy-1,4-naphthoquinone) in the presence of the hypoxanthine/xanthine oxidase system

JOURNAL OF APPLIED TOXICOLOGY, Issue 4 2003
A. M. Osman
Abstract This study reports that lawsone (2-hydroxy-1,4-naphthoquinone) undergoes redox cycling in the presence of the hypoxanthine/xanthine oxidase system. The rate of cytochrome c reduction obtained in the presence of 80 µM lawsone was almost three times the rate of cytochrome c reduction measured in its absence. This increase in the rate of cytochrome c reduction was partially inhibited by superoxide dismutase, suggesting the involvement of O2,, in this process. It is remarkable to note that, even though lawsone is considered to be a non-redox-cycling quinone in vitro, this quinone was shown to be more toxic in vivo in rats than menadione, causing haemolytic anemia of an oxidative nature and renal damage. The view that this quinone is a non-redox-cycling quinone was based on the inability of one-electron-transferring ,avoenzymes such as NADPH-cytochrome c reductase to reduce this naphthoquinone. Our ,nding that lawsone, like menadione, undergoes redox cycling in the presence of the hypoxanthine/xanthine oxidase system could explain the observed oxidative damage of tissues in,icted by this quinone in rats in vivo. Such an observation therefore reconciles the in vivo toxicity results of this naphthoquinone with those of in vitro experiments. Copyright © 2003 John Wiley & Sons, Ltd. [source]


Regulation of angiotensin II-stimulated osteopontin expression in cardiac microvascular endothelial cells: Role of p42/44 mitogen-activated protein kinase and reactive oxygen species,

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 1 2001
Zhonglin Xie
Using spontaneously hypertensive and aortic banded rats, we have shown that expression of myocardial osteopontin, an extracellular matrix protein, coincides with the development of heart failure and is inhibited by captopril, suggesting a role for angiotensin II (ANG II). This study tested whether ANG II induces osteopontin expression in adult rat ventricular myocytes and cardiac microvascular endothelial cells (CMEC), and if so, whether induction is mediated via activation of mitogen-activated protein kinases (p42/44 MAPK) and involves reactive oxygen species (ROS). ANG II (1 ,M, 16 h) increased osteopontin expression (fold increase 3.3±0.34, n,=,12, P,<,0.01) in CMEC as measured by northern analysis, but not in ARVM. ANG II stimulated osteopontin expression in CMEC in a time- (within 4 h) and concentration-dependent manner, which was prevented by the AT1 receptor antagonist, losartan. ANG II elicited robust phosphorylation of p42/44 MAPK as measured using phospho-specific antibodies, and increased superoxide production as measured by cytochrome c reduction and lucigenin chemiluminescence assays. These effects were blocked by diphenylene iodonium (DPI), an inhibitor of the flavoprotein component of NAD(P)H oxidase. PD98059, an inhibitor of p42/44 MAPK pathway, and DPI each inhibited ANG II-stimulated osteopontin expression. Northern blot analysis showed basal expression of p22phox, a critical component of NADH/NADPH oxidase system, which was increased 40,60% by exposure to ANG II. These results suggest that p42/44 MAPK is a critical component of the ROS-sensitive signaling pathways activated by ANG II in CMEC and plays a key role in the regulation of osteopontin gene expression. Published 2001 Wiley-Liss, Inc. [source]


Ethanol Can Modify the Effects of Certain Free Radical-Generating Systems on Astrocytes

ALCOHOLISM, Issue 4 2004
B. Gonthier
Abstract: The central nervous system is vulnerable to oxidative stress, especially when a toxicant can modify the physiological balance between anti- and pro-oxidant mechanisms. Among brain cells, astrocytes seem less vulnerable than neurons, but their impairment can dramatically affect neurons because of their protective role toward neurons. Ethanol is able to stimulate the formation of reactive oxygen species and modify the activity of most of the antioxidant agents. However, ethanol can react with the OH· radical to form the ,-hydroxyethyl radical, which is considered to be less toxic. Ethanol also can stimulate H2O2 degradation through catalase activation. This study, therefore, sought to determine whether ethanol affected the sensitivity of astrocytes exposed to various free radical-generating systems. The cellular impact of such exposure was assessed by assays exploring cytotoxicity (i.e., NR (neutral red) and MMT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetiazolium bromide) reduction assays) and genotoxicity (comet assay) induced by these treatments. DNA alterations were evaluated by single-cell gel electrophoresis (comet assay), considered a precocious biomarker of intracellular alterations. After concomitant exposure to H2O2 and ethanol, the viability of astrocytes decreased significantly whereas the mean percentage of DNA in the tail increased, reflecting DNA damage (H2O2 was either directly added to the culture medium or endogenously produced from menadione). Ethanol also reduced the loss of viability and DNA alterations after exposure to OH· radicals produced by a Fenton system. The exposure to a xanthine/xanthine oxidase system had the same effect. [source]


Teratogenicity of antiepileptic drugs: role of drug metabolism and pharmacogenomics

ACTA NEUROLOGICA SCANDINAVICA, Issue 1 2007
R. Sankar
The approach to clinical decision-making pertaining to the use of antiepileptic drugs (AEDs) during pregnancy has relied on previous accumulated experience and, since the 1990s, on data from pregnancy registries. The limitations of this process are that no information regarding the chemical attributes of the AED under consideration, nor the role of a number of enzyme systems that are known to interact with foreign compounds to modify their potential for harm, are included. The role of the hepatic mixed function oxidase system may be especially important in conferring teratogenic risk. However, systems such as epoxide hydrolase, glutathione reductase, superoxide dismutase and other toxin-scavenging systems may be important modifiers that lower the risk. Knowledge is also accumulating on the interactions of AEDs with molecular targets such as histone deacetylase and peroxisome proliferator-activated receptors that may play important roles in teratogenesis. While our knowledge of these factors are incomplete, progress can be achieved by beginning to include these concepts in our discussion on the topic and by promoting research that may improve our ability to individualize the analysis of risk for a specific patient with regards to specific AEDs. [source]


NADH/NADPH oxidase p22 phox C242T polymorphism and lipid peroxidation in coronary artery disease

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2001
O. Stanger
The nicotinamide adenine dinucleotide (NADH)/nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system is a major source of superoxide anion (·O2,) production in the human vasculature and may therefore influence lipid peroxidation and severity of atherosclerosis. This study aimed to investigate a hypothetical influence of the p22 phox C242T polymorphism on the generation of malondialdehyde (MDA), extent and clinical onset of coronary artery disease (CAD) in patients. We studied 108 male Caucasians with angiographically documented CAD and 45 controls free of vascular disease under 60 years of age. p22 phox C242T genotypes and MDA levels were determined. Additional information was obtained from each subject on classic risk factors and clinical events of CAD. Genotype distribution in CAD-patients and controls was thymine,thymine (TT): 13·8% (13·3%), cytosine,thymine (CT): 46·3% (53·3%) and cytosine,cytosine (CC): 39·8% (33·3%), respectively. No significant influence was seen of the p22 phox C242T polymorphism on corresponding mean MDA levels in both groups. Furthermore, age at onset of first time angina pectoris (AP) and myocardial infarction (MCI) was not significantly different between genotype groups. It is concluded that the C242T polymorphism of the p22 phox gene is not associated with lipid peroxidation as measured by MDA, and is not a genetic risk marker for CAD Caucasians. [source]