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phosphatidyl serine/nekrose
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Apoptosis in esophagus and pancreas carcinoma cells induced by circulating microparticles is related to phosphatidyl serine and microparticle-associated caspases.
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Circulating microparticles (MPs) are recently discussed as "biologically active", participating in the pathology of diseases rather than being a marker of damaging processes. It was the purpose of the present study to investigate the effects of MPs, as isolated from the blood of healthy volunteers,
Clinical dose of lidocaine destroys the cell membrane and induces both necrosis and apoptosis in an identified Lymnaea neuron.
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OBJECTIVE
Although lidocaine-induced cell toxicity has been reported, its mechanism is unclear. Cell size, morphological change, and membrane resistance are related to homeostasis and damage to the cell membrane; however, the effects of lidocaine on these factors are unclear. Using an identified
Blood cell apoptosis/necrosis: some clinical and laboratory aspects.
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Exposure of phosphatidyl-serine on blood cell membrane surface and microvesiculation as the hallmarks of apoptosis/necrosis were investigated. The effect of leukofiltration on the retention/generation of microvesicules, leukocyte subsets and major biological response modifiers were evaluated in a
Comparison of anthracycline-induced death of human leukemia cells: programmed cell death versus necrosis.
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We investigated the mode of cell death induced by the anthracyclines, aclarubicin, doxorubicin and daunorubicin in the human leukemia cell lines, HL60 and Jurkat. The cells were incubated with drug concentrations up to 500 nM for periods between 3 and 24 hours, followed by morphological and
Interleukin-2-activated natural killer cells can induce both apoptosis and necrosis in rat hepatocytes.
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Natural killer (NK) cells play a crucial role in the elimination of virus-infected or transformed cells in the liver. In this article, we describe the mechanism by which liver cells are killed by NK cells. Interleukin-2-activated natural killer (A-NK) cells from the rat induced apoptotic cell death
Different and synergistic actions of human tumor necrosis factor and interferon-gamma in damage of liposome membranes.
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The effects of human recombinant tumor necrosis factor (TNF) and interferon-gamma (IFN-gamma) in damage of liposome membranes were examined to elucidate the molecular mechanism of their antiproliferative actions on tumor cells. The extent of membrane damage was assayed by measuring the rate of
Kahalalide F induces necrosis-like cell death that involves depletion of ErbB3 and inhibition of Akt signaling.
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Kahalalide F (KF) is a novel marine-derived antitumor agent that is currently undergoing phase II clinical trials. The mechanism of action of KF is not well understood. In line with previous reports, we show that KF caused rapid and potent cytotoxicity in the breast cancer cell lines SKBR3 and
Tumor necrosis factor alpha induces a caspase-independent death pathway in human neutrophils.
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Tumor necrosis factor alpha (TNF-alpha) is a cytokine with multiple roles in the immune system, including the induction and potentiation of cellular functions in neutrophils (PMNs). TNF-alpha also induces apoptotic signals leading to the activation of several caspases, which are involved in
Silica phagocytosis causes apoptosis and necrosis by different temporal and molecular pathways in alveolar macrophages.
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Chronic inhalation of crystalline silica is an occupational hazard that results in silicosis due to the toxicity of silica particles to lung cells. Alveolar macrophages play an important role in clearance of these particles, and exposure of macrophages to silica particles causes cell death and
Aluminum-maltolate induces apoptosis and necrosis in neuro-2a cells: potential role for p53 signaling.
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Aluminum maltolate (Al-malt) causes neurodegeneration following in vivo exposure, and apoptosis plays a prominent role. The objective of this study was to define the form of cell death induced by Al-malt and to establish an in vitro model system amenable to mechanistic investigations of
Antiproliferative property of n-hexane and chloroform extracts of Anisomeles malabarica (L). R. Br. in HPV16-positive human cervical cancer cells.
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OBJECTIVE
To find the efficacy of serial extracts of Anisomeles malabarica in inhibiting proliferation of and inducing apoptosis in human cervical cancer cells, SiHa and ME 180, that are HPV 16-positive.
METHODS
The whole plant was extracted in n-hexane, chloroform, ethyl acetate, n-butanol,
IgA1 protease from Neisseria gonorrhoeae inhibits TNFalpha-mediated apoptosis of human monocytic cells.
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The modulation of programmed cell death is a common theme in the patho-physiology of inflammation and infectious disease. The synthesis and secretion of an IgA1 protease is strictly associated with virulence of the Neisseria species. Here, we report on the inhibition of tumor necrosis factor alpha
Use of flow cytometry in an apoptosis assay to determine pH and temperature stability of shiga-like toxin 1.
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Shiga toxins and Shiga-like toxins (Stx) are a relatively large group of cytotoxins produced by certain serotypes of Shigella and E. coli (STEC). These toxins are responsible for diarrhea, hemorrhagic colitis and may induce hemolytic uremic syndrome (HUS) with serious consequences in young children.
Neuroprotective actions of Selegiline in inhibiting 1-methyl, 4-phenyl, pyridinium ion (MPP+)-induced apoptosis in SK-N-SH neurons.
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We have examined mitochondrial membranes and molecular hallmarks of apoptosis in response to increasing concentrations of 1-Methyl, 4-phenyl, Pyridinium ion (MPP(+)) in SK-N-SH neurons and have evaluated the neuroprotective potential of Selegiline with a primary objective to explore its mechanism(s)
Induction of Apoptosis in Rat Peripheral Blood Lymphocytes by the Anticancer Drug CI-994 (Acetyldinaline)(*).
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CI-994 (acetyldinaline) is an investigational anticancer drug currently in clinical trials. In preclinical safety studies in rats and dogs, CI-994 resulted in significant toxicity to bone marrow and lymphoid tissue. To determine if apoptosis was involved in CI-994 toxicity, peripheral blood
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