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peroxidase/nécrose
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Increased erythrocyte glutathione peroxidase activity and serum tumor necrosis factor-alpha in HIV-infected patients: relationship to on-going prothrombotic state.
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A condition of oxidative stress, due to perturbation of oxidant/antioxidant balance, has been suggested to play a role not only in the pathogenesis of human immunodeficiency virus (HIV) infection, but also in the promotion of a thrombophilic condition. Because various hemostatic dysfunctions usually
A peroxidase-linked enzyme immunoassay for tumour necrosis factor alpha utilising alternative colorimetric or chemilumimetric substrates.
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We present a double antibody immunoassay for tumour necrosis factor alpha (TNF alpha) with a peroxidase dependent endpoint which can be detected by absorbance or chemiluminescence depending on the choice of substrate. The chemilumimetric and colorimetric assays have a detection threshold in human
Increased expression of tumor necrosis factor-alpha and decreased expression of thyroglobulin and thyroid peroxidase mRNA levels in the thyroids of iodide-treated BB/Wor rats.
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Several lines of evidence suggest that tumor necrosis factor-alpha (TNFalpha) may contribute to the pathogenesis of autoimmune thyroid disease. It is not known, however, whether increased thyroidal TNFalpha levels are associated with changes in thyroid function. The purpose of the present study was
Peroxidases enhance macrophage-mediated cytotoxicity via induction of tumor necrosis factor.
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Tumor necrosis factor (TNF) is a monokine which is involved in macrophage-mediated cytotoxicity (MMC). We have previously reported that peroxidases can activate thioglycollate-induced macrophages to the tumoricidal state in vitro. The present study was undertaken in an attempt to correlate
Tumor necrosis factor-alpha and interferon-gamma modulate gene expression of type I 5'-deiodinase, thyroid peroxidase, and thyroglobulin in FRTL-5 rat thyroid cells.
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Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) have many effects on a number of cell types, including thyrotrophs. In the present study, we used FRTL5 cells, a cultured rat thyroid follicular cell line, to examine the effects of IFN-gamma and TNF-alpha on type I
Serological relationships between tobacco necrosis virus-inducible cucumber peroxidase and corresponding peroxidase isoenzymes in other Cucurbitaceae.
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Pathogenesis-related peroxidases (PRXs), found in leaves of different cucurbits infected with tobacco necrosis virus (TNV), were compared serologically using a highly specific rabbit antiserum raised against PRX purified from TNV-infected cotyledons of Cucumis sativus L., cv. Laura. After native
Arabidopsis thaliana deficient in two chloroplast ascorbate peroxidases shows accelerated light-induced necrosis when levels of cellular ascorbate are low.
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Arabidopsis chloroplasts have a multi-layered defense against hydrogen peroxide (H(2)O(2)) that includes a stromal and thylakoid ascorbate peroxidase (sAPX and tAPX). Single and double null mutants in SAPX and TAPX (sapx and tapx) were each crossed with ascorbate deficient vtc2. The single, double
Human eosinophil peroxidase enhances tumor necrosis factor and hydrogen peroxide release by human monocyte-derived macrophages.
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Inhibition of growth or eradication of experimentally induced tumors has been shown to be accompanied by infiltration of eosinophils and macrophages into the tumor mass. Since macrophages are important mediators of host antitumor activity, the possibility arises that a collaboration may exist
Attenuating tumor necrosis factor alpha does not ameliorate other cytokine and peroxidase products during sepsis.
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BACKGROUND
Recent trials utilizing single anticytokine agents have shown no consistent survival benefit in improving the outcome of sepsis. Since an entire cascade of mediators contributes to the underlying pathophysiology, it is not surprising that monotherapy has proven unsuccessful. The purpose
Mitogenic actions of peroxidase proliferators: involvement of protein kinase C and tumor necrosis factor alpha.
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Glutathione peroxidase system and microsomal lipoperoxidation in prenecrotic stages of dietary hepatic necrosis in rats.
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Induction of cellular necrosis by the glutathione peroxidase mimetic ebselen.
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The selenium-based compound ebselen is a powerful antioxidant, a potent anti-inflammatory agent and a potential neuroprotective compound. Several studies have demonstrated that part of the biological effect of ebselen is the result of the inhibition of apoptosis. We show in this report that ebselen
Tumor necrosis factor-alpha (TNF-alpha) in loosening of total hip replacement (THR).
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OBJECTIVE
The initially well-fixed implants of total hip replacement (THR) are in the long-term subject to aseptic loosening. Many cytokines can contribute to osteolysis due to osteoclast recruitment and/or activation. However, in this respect tumor necrosis factor-alpha (TNF-alpha) plays a pivotal
Radiosurgery-induced microvascular alterations precede necrosis of the brain neuropil.
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OBJECTIVE
Radiosurgery is used as a therapeutic modality for a wide range of cerebral disorders. It is important to understand the underlying causes of deleterious side effects that may accompany gamma-irradiation of brain tissue. In this study, structural alterations in rat cerebral vessels
Glutathione peroxidase-deficient mice are more susceptible to neutrophil-mediated hepatic parenchymal cell injury during endotoxemia: importance of an intracellular oxidant stress.
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Neutrophils contribute to hepatocellular injury in a number of acute inflammatory reactions. However, the molecular mechanism of parenchymal cell injury remains controversial. To address the issue of whether or not reactive oxygen species (ROS) are important in the injury process, we used the
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