tellurium/necrosis

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Necrosis of schwann cells during tellurium-induced primary demyelination: DNA fragmentation, reorganization of splicing machinery, and formation of intranuclear rods of actin.

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We present a cytological, immunocytochemical, and biochemical study of the cell death of mature myelinating Schwann cells (SCs) in the primary demyelinating neuropathy induced by tellurium (Te). Weaned rats were fed a diet containing 1.1% elemental Te. The animals were killed daily within the first

Evaluation of tellurium toxicity in transformed and non-transformed human colon cells.

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Diphenyl ditelluride (DPDT) and tellurium tetrachloride (TeCl(4)) were evaluated for toxicity in transformed (HT-29, Caco-2) and non-transformed colon cells (CCD-18Co). Significant decreases in viability were observed with DPDT exposure in HT-29 (62.5-1000 μM), Caco-2 (31.25-1000 μM) and CCD-18Co

Cytotoxicity investigations of biogenic tellurium nanorods towards PC12 cell line.

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The authors evaluated the cytotoxicity underlying mechanisms of biogenic tellurium (Te) nanorods (NRs) produced by the Pseudomonas pseudoalcaligenes strain Te on the PC12 cell line. The half-maximal inhibitory concentration (IC₅₀) value was estimated at 5.05 ± 0.07 ng/ml for

Effect of 2-TeCD on the expression of adhesion molecules in human umbilical vein endothelial cells under the stimulation of tumor necrosis factor-alpha.

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Adhesion molecules play an important role in the pathogenesis of atherogenesis. They are expressed on endothelial cells surface in response to various inflammatory stimuli. In this paper, we examined the effect of 2-tellurium-bridged beta-cyclodextrin (2-TeCD), a GPx mimic, on the expression of

2-Tellurium-bridged β-cyclodextrin, a thioredoxin reductase inhibitor, sensitizes human breast cancer cells to TRAIL-induced apoptosis through DR5 induction and NF-κB suppression.

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) exhibits potent antitumor activity via membrane receptors on cancer cells without deleterious side effects for normal tissue. Unfortunately, breast cancer cells, as many other cancer types, develop resistance to TRAIL; therefore, TRAIL

Induction of lesions of selenium-vitamin E deficiency in weanling swine fed silver, cobalt, tellurium, zinc, cadmium, and vanadium.

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Forty-two weanling pigs were allotted to 7 groups and fed (for 10 weeks) a commercial ration that was adequate in selenium and vitamin E (Se-E) content, either alone or with supplements of Ag (3,000 mg/kg of feed, as acetate), Co (500 mg/kg, as chloride), Te (500 mg/kg, as tetrachloride), Zn (3,000

Resolution of inflammation-related apoptotic processes by the synthetic tellurium compound, AS101 following liver injury.

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OBJECTIVE Fulminant hepatic failure is a dangerous condition, which occurs when large parts of the liver become damaged beyond repair, and the liver is no longer able to function. This syndrome is induced by inflammatory processes, resulting in acute liver failure. Recently, the organotellurium

Myocardial ultrastructural alterations in ducklings fed tellurium.

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Seventy newly hatched ducklings were fed a commercial ration with 500 mg of added Te (as tetrachloride)/kg of feed for up to 28 days. Ducklings were euthanatized at day 14, 21, and 28, the hearts were studied by gross, microscopic, and ultrastructural examination. Cardiac damage was apparent grossly

Induction of lesions of selenium-vitamin E deficiency in ducklings fed silver, copper, cobalt, tellurium, cadmium, or zinc: protection by selenium or vitamin E supplements.

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In 3 experiments, 684 newly hatched White Pekin ducklings were fed (for 15 to 28 days) a commercial starter mash that was adequate in selenium and vitamin E (Se-E) content, either alone or with supplements of Ag (3,000 mg/kg of feed, as acetate), Cu (1,500 mg/kg, as sulfate), Co (200 or 500 mg/kg,

Reversible near-infrared fluorescent probe introducing tellurium to mimetic glutathione peroxidase for monitoring the redox cycles between peroxynitrite and glutathione in vivo.

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The redox homeostasis between peroxynitrite and glutathione is closely associated with the physiological and pathological processes, e.g. vascular tissue prolonged relaxation and smooth muscle preparations, attenuation hepatic necrosis, and activation matrix metalloproteinase-2. We report a

Diphenyl ditelluride intoxication triggers histological changes in liver, kidney, and lung of mice.

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Tellurium compounds may be cytotoxic to different cells types. Thus, this work evaluated the effect of diphenyl ditelluride ((PhTe)2), an organotellurium commonly used in organic synthesis, on the morphology of liver, kidney, and lung. Adult mice were acutely (a subcutaneous single dose: 250

Telluric acid ameliorates hepatic ischemia reperfusion-induced injury in rats: Involvement of TLR4, Nrf2, and PI3K/Akt signaling pathways.

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In past tellurium-based compounds had limited use, however, their therapeutic potential have been target of interest recently due to antioxidant and anti-inflammatory capabilities in experimental endotoxemia. Nevertheless, their potential hepatoprotective effect against ischemia reperfusion (IR)

Isotopologous Organotellurium Probes Reveal Dynamic Hypoxia In Vivo with Cellular Resolution.

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Changes in the oxygenation state of microenvironments within solid tumors are associated with the development of aggressive cancer phenotypes. Factors that influence cellular hypoxia have been characterized; however, methods for measuring the dynamics of oxygenation at a cellular level in vivo have

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