Cytoskeleton as a target in menadione-induced oxidative stress in cultured mammalian cells: Alterations underlying surface bleb formation

Malorni, Walter; Iosi, Francesca; Mirabelli, Francesca; Bellomo, Giorgio

doi:10.1016/0009-2797(91)90026-4

Cited by 109 publications

(56 citation statements)

References 36 publications

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“…These cytoskeletal structure proteins are targets for oxidative stress; they may also represent markers of neuronal density, synaptosomal structure and dendritic spines. 38 The findings discussed above and the change of brain proteins associated with neuronal migration and axonal outgrowth in our rodent model outlined earlier indicate hyperoxia-induced morphological alterations like the formation of aberrant axons and dendrites and/or a loss of neuronal polarity. Anatomical abnormalities such as mossy fiber sprouting and the formation of additional and abnormal synaptic connections have been observed in response to repeated early-life seizures.…”

Section: Neuronal Differentiation Migration Axonal Growth and Guidancementioning

confidence: 56%

Acute and long-term proteome changes induced by oxidative stress in the developing brain

et al. 2005

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The developing mammalian brain experiences a period of rapid growth during which various otherwise innocuous environmental factors cause widespread apoptotic neuronal death. To gain insight into developmental events influenced by a premature exposure to high oxygen levels and identify proteins engaged in neurodegenerative and reparative processes, we analyzed mouse brain proteome changes at P7, P14 and P35 caused by an exposure to hyperoxia at P6. Changes detected in the brain proteome suggested that hyperoxia leads to oxidative stress and apoptotic neuronal death. These changes were consistent with results of histological and biochemical evaluation of the brains, which revealed widespread apoptotic neuronal death and increased levels of protein carbonyls. Furthermore, we detected changes in proteins involved in synaptic function, cell proliferation and formation of neuronal connections, suggesting interference of oxidative stress with these developmental events. These effects are age-dependent, as they did not occur in mice subjected to hyperoxia in adolescence.

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Section: Neuronal Differentiation Migration Axonal Growth and Guidancementioning

confidence: 56%

Acute and long-term proteome changes induced by oxidative stress in the developing brain

et al. 2005

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“…The cytoskeleton has been shown to be involved in oncosis and plasma membrane permeability [20,21,28] . The depletion of cytoskeleton-associated proteins can break the membrane cytoskeleton linkage and decrease the physical support of the basal plasma membrane, leading to bleb formation and increased membrane permeability.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have suggested that surface bleb formation and plasma membrane integrity are related to alterations of the cytoskeletal network [20][21][22] . In the current study, immunocytochemical investigations revealed changes in the cytoskeletal network of fluopsin C-exposed cells.…”

Section: Fluopsin C Destroyed the Cell Skeletonmentioning

confidence: 99%

Fluopsin C induces oncosis of human breast adenocarcinoma cells

Jiang

Cui

et al. 2013

Acta Pharmacol Sin

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Aim: Fluopsin C, an antibiotic isolated from Pseudomonas jinanesis, has shown antitumor effects on several cancer cell lines. In the current study, the oncotic cell death induced by fluopsin C was investigated in human breast adenocarcinoma cells in vitro. Methods: Human breast adenocarcinoma cell lines MCF-7 and MD-MBA-231 were used. The cytotoxicity was evaluated using MTT assay. Time-lapse microscopy and transmission electron microscopy were used to observe the morphological changes. Cell membrane integrity was assessed with propidium iodide (PI) uptake and lactate dehydrogenase (LDH) assay. Flow cytometry was used to measure reactive oxygen species (ROS) level and mitochondrial membrane potential (Δψm). A multimode microplate reader was used to analyze the intracellular ATP level. The changes in cytoskeletal system were investigated with Western blotting and immunostaining.Results: Fluopsin C (0.5-8 μmol/L) reduced the cell viability in dose-and time-dependent manners. Its IC 50 values in MCF-7 and MD-MBA-231 cells at 24 h were 0.9 and 1.03 μmol/L, respectively. Fluopsin C (2 μmol/L) induced oncosis in both the breast adenocarcinoma cells characterized by membrane blebbing and swelling, which was blocked by pretreatment with the pan-caspase inhibitor Z-VAD-fmk. In MCF-7 cells, fluopsin C caused PI uptake into the cells, significantly increased LDH release, induced cytoskeletal system degradation and ROS accumulation, decreased the intracellular ATP level and Δψm. Noticeably, fluopsin C exerted comparable cytotoxicity against the normal human hepatocytes (HL7702) and human mammary epithelial cells with the IC 50 values at 24 h of 2.7 and 2.4 μmol/L, respectively. Conclusion: Oncotic cell death was involved in the anticancer effects of fluopsin C on human breast adenocarcinoma cells in vitro. The hepatoxicity of fluopsin C should not be ignored.

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“…As a result, redox cycling can ensue and produce large amounts of superoxide, which can dismutate to form H 2 O 2 or form more toxic ROS via intracellular metal-catalyzed reactions (O'Brien, 1991;Venugopal et al, 1996aVenugopal et al, , 1996bJamison et al, 2001Jamison et al, , 2002Jamison et al, , 2004. This redox cycling generates oxidative stress (Bellomo et al, 1982;Cohen and Slubberfield, 1990) and results in a number of deleterious effects on T24 cells, including depletion of NADPH (Akman et al, 1985) and reduced glutathione (Carbonera and Azzone, 1988;Bellomo et al, 1990;Cohen and Stubberfield, 1990;Fawthrop et al, 1991) with the oxidation of sulfhydryl groups in proteins, especially microtubules and other cytoskeletal proteins, such as the cytokeratins (Bellomo et al, 1990;Malorni et al, 1991;Wu et al, 1993aWu et al, , 1993bJarabak and Jarabak, 1995). Even minor quinone-induced peroxidation can damage cellular calcium transport systems and result in excess intracellular Ca 2ϩ levels that can also damage the cells.…”

Section: Menadione Cytotoxicitymentioning

confidence: 99%

“…As a result of this cytoskeletal damage, only a few long filopodial extensions were found (Svikina et al, 2003). Damage to the cytoskeletal architecture was also reflected by the formation of lamellar cytoplasm, large blebs followed by excisions and acute distortions in T24 cell shape (Malorni et al, 1991). Mitochondria showed intramatrical densities and high contrast (at least in the mitochondrial profiles viewed in the perikaryon).…”

Section: Menadione Cytotoxicitymentioning

confidence: 99%

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Gilloteaux¹,

Jamison²,

Arnold³

et al. 2005

Anat. Rec.

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Feulgen and actin-phalloidin staining as well as gel electrophoresis have been employed in conjunction with cell ultrastructure to describe the effects of 1-, 2-, and 4-hr ascorbate (VC), menadione (VK 3 ), and ascorbate:menadione (VC:VK 3 ) treatments on the T24 human bladder carcinoma cell line. T24 cells exposed to VC alone display blebs and other superficial membrane defects related to membrane alterations and to superficial cytoskeleton changes. VK 3 treatment damages the cell nucleus and organelles, leads to the redistribution of the organelles in the perikaryon as a consequence of cytoskeletal damage, and results in cytoplasmic self-excisions. After VC:VK 3 treatment, the cells show exaggerated alterations characteristic of each vitamin treatment alone, including damaged mitochondria, self-excision of organelle-free pieces of cytoplasm, and extrusion of the perikaryon containing a nucleus surrounded by the damaged organelles. The nuclear envelope appears intact and contains chromatin that decondenses and dissipates. During the cellular demise that concludes with apparent karyolysis, the cells significantly decrease their size and alter their shape. However, the cisterns of rough endoplasmic reticulum are undamaged, but may become dilated. Since the cellular phenomena leading to cell death differ morphologically from apoptosis and necrosis, but entail selfcutting without nuclear bodies, this new form of cell death was called autoschizis. In addition, gel electrophoresis and Feulgen staining demonstrate that autoschizis is accompanied by random DNA degeneration.

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Cytoskeleton as a target in menadione-induced oxidative stress in cultured mammalian cells: Alterations underlying surface bleb formation

Cited by 109 publications

References 36 publications

Acute and long-term proteome changes induced by oxidative stress in the developing brain

Acute and long-term proteome changes induced by oxidative stress in the developing brain

Fluopsin C induces oncosis of human breast adenocarcinoma cells

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

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