arsenic/نخر

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Arsenic induces tumor necrosis factor alpha release and tumor necrosis factor receptor 1 signaling in T helper cell apoptosis.

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Long-term exposure to arsenic induces arsenical cancers in human beings. Arsenic has been shown to induce apoptosis in a variety of cell systems. Previous studies revealed that patients with arsenic-induced Bowen's disease showed a defective cell-mediated immunity and decreased percentages of T cell

[Arsenic trioxide resulting in alveolar bone chemical necrosis: report of 2 cases].

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The most serious complication of arsenic trioxide devitalization of dental pulp is alveolar bone chemical necrosis because of iatrogenic perforation of pulp chamber and arsenic trioxide leakage. Arsenic trioxide is protoplasmic poison.When it contacts periodontal tissues, alveolar bone degeneration,

Effect of Arsenic Trioxide in TRAIL (Tumor Necrosis Factor-related Apoptosis Inducing Ligand)-Mediated Apoptosis in Multiple Myeloma Cell Lines.

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OBJECTIVE The potential therapeutic application of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), in the treatment of multiple myeloma (MM), was recently proposed. However, there have been some problems with the use of TRAIL, due to the appearance of TRAIL-resistant cells in

Effect of thalidomide and arsenic trioxide on the release of tumor necrosis factor-α and vascular endothelial growth factor from the KG-1a human acute myelogenous leukemia cell line.

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Studies conducted in our lab have indicated that thalidomide cytotoxicity in the KG-1a human acute myelogenous leukemia (AML) cell line was enhanced by combining it with arsenic trioxide. The current investigation was conducted in order to evaluate the effect of thalidomide either alone or in

Bone marrow necrosis in a patient with acute promyelocytic leukemia during re-induction therapy with arsenic trioxide.

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Arsenic trioxide (As2O3) therapy at a daily dose of 0.15 mg/kg was given to a 60-yr-old Japanese male with refractory acute promyelocytic leukemia. White blood cell (WBC) of 6.6 x 10(3)/microl increased to 134 x 10(3)/microl following the administration of As2O3. Daily hydroxyurea (HU), and

Prenatal arsenic exposure and shifts in the newborn proteome: interindividual differences in tumor necrosis factor (TNF)-responsive signaling.

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Exposure to inorganic arsenic (iAs) early in life is associated with adverse health effects in infants, children, and adults, and yet the biological mechanisms that underlie these effects are understudied. The objective of this research was to examine the proteomic shifts associated with prenatal

Arsenic suppresses necrosis induced by selenite in human leukemia HL-60 cells.

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Selenium, an essential trace element for humans, has been shown to have anticancer effects. Arsenic, a possibly essential ultratrace element for humans, has been used in the treatment of leukemia. Anticancer effects of selenium and arsenic have been related to their ability to induce apoptosis.

Management of arsenic trioxide necrosis in the maxilla.

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Historically, pulp-necrotizing agents were commonly used in endodontic treatments. They act quickly and devitalize the pulp within a few days. However, they are cytotoxic to gingiva and bone. If such an agent diffuses out of the cavity, it can readily cause widespread necrosis of gingiva and bone,

Arsenic trioxide-induced osteo-necrosis treatment in a child: mini-review and case report.

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BACKGROUND Arsenic oxide compounds were traditionally used as devitalizing agents. Due to its toxicity, leakage of such compounds into the periodontium can cause gingival and osteo-necrosis. Their use is forbidden in Europe and the USA for decades, however, some dentists seem to still use

Gingival and localized alveolar bone necrosis related to the use of arsenic trioxide paste--two case reports.

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The leakage of arsenic trioxide paste from tooth fillings has been associated with widespread necrosis of the supporting periodontal tissues. This report describes two cases of arsenic trioxide paste-induced gingival and localized alveolar bone necrosis in the mandible, following the use of arsenic

Mandibular bone necrosis caused by use of arsenic paste during endodontic treatment: two case reports.

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OBJECTIVE To report that arsenical pastes are still employed in endodontics and to highlight the potentially serious consequences of their use. CONCLUSIONS Chemotherapeutic agents such as arsenic trioxide and paraformaldehyde were once commonly employed as pulp-necrotizing agents. Their cytotoxic

Chronic renal insufficiency from cortical necrosis induced by arsenic poisoning.

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A 39-year-old man had anuria and azotemia and was found to be suffering from acute arsenic poisoning. After two peritoneal dialyses, partial renal function returned, and the patient has survived for five years without dialysis. Renal cortical necrosis was demonstrated by renal biopsy and renal

Arsenic trioxide (As(2)O(3)) induces apoptosis and necrosis mediated cell death through mitochondrial membrane potential damage and elevated production of reactive oxygen species in PLHC-1 fish cell line.

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Several environmental pollutants, including metals can induce toxicological effect on aquatic animal species. Most studies to understand the toxicity of arsenic compounds were performed in mammalian cells; however, the study of the arsenic toxicity to the aquatic animals' species, including fish, is

Atypical blasts and bone marrow necrosis associated with near-triploid relapse of acute promyelocytic leukemia after arsenic trioxide treatment.

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The pathologic features of acute promyelocytic leukemia (APL) with t(15;17)(q22;q21) are highly characteristic, which with few exceptions enable a firm diagnosis to be made on morphologic grounds. An APL patient in first relapse presented with large, bizarre circulating blasts and bone marrow

Arsenic trioxide causes selective necrosis in solid murine tumors by vascular shutdown.

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To investigate the antitumor action of arsenic trioxide in solid tumors, we carried out quantitative tumor perfusion studies, using locally advanced methylcholanthrene-induced fibrosarcoma grown in BALB/c mice. The tumor perfusion studies were assessed by two separate methods: 99mTc clearance and

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