Lipid peroxidation and morphological changes in mammalian cells treated with the glutathione oxidant, diamide*1

Power, Judith A.; Harris, J. W.; Bainton, Dorothy F.

doi:10.1016/0014-4827(77)90142-2

Cited by 17 publications

(7 citation statements)

References 22 publications

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“…At higher doses of the oxidant, zygotes do start the apoptotic process, as evidenced by the appearance of cell shrinkage. This process might be earlier than cell cycle arrest but cannot be completed before necrosis takes place, which may be due to extensive lipid peroxidation [34], leading to destruction of the cell membrane and thus increased permeability to PI stain. Our results suggest that thiol oxidation plays an important role in zygotic cell death and that the intensity of oxidative stress may determine which death pathway is triggered.…”

Section: Discussionmentioning

confidence: 98%

Thiol Oxidation-Induced Embryonic Cell Death in Mice Is Prevented by the Antioxidant Dithiothreitol1

Liu

Trimarchi

Keefe

1999

Biology of Reproduction

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The oxidation of cellular sulfhydryl (SH) groups has been implicated in the induction of apoptosis in various types of cells and in the disturbance of the meiotic spindle of murine oocytes during aging. The objective of this study was to determine whether the SH-specific oxidant diamide could inhibit embryo development and induce cell death, and whether the antioxidant dithiothreitol (DTT) could counteract such effects. Exposure of mouse zygotes to diamide for 3 h at 25 or 50 microM (but not 12.5 microM) resulted in cell cycle arrest and cell death with evidence of apoptosis. At higher concentrations (100 or 200 microM), diamide induced necrosis as evidenced by propidium iodide-positive pronuclei within 24 h of treatment. Simultaneous addition of DTT at equimolar concentration prevented these effects. However, when DTT was added later, it was no longer protective. DTT also effectively protected against the thiol-oxidative damage caused by diamide in blastocysts. These results suggest that altering thiol-redox status in zygotes and blastocysts may result in cell cycle arrest, apoptosis, and/or cell death.

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Section: Discussionmentioning

confidence: 98%

Thiol Oxidation-Induced Embryonic Cell Death in Mice Is Prevented by the Antioxidant Dithiothreitol1

Liu

Trimarchi

Keefe

1999

Biology of Reproduction

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“…Scott et al (20) observed that treatment of cells with a variety of sulfhydryl reagents resulted in the release of membrane vesicles. Indeed, examination of the literature reveals numerous instances in which treatment of cells with sulfhydryl modifiers resulted in-membrane blebbing (28,29). Scott et al (30) observed that the membrane components present in the released vesicles were not selective but represented a random distribution of membrane polypeptides.…”

Section: Discussionmentioning

confidence: 99%

Phenylarsine oxide-induced increase in alveolar macrophage surface receptors: evidence for fusion of internal receptor pools with the cell surface.

Kaplan

Wiley

1985

The Journal of Cell Biology

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Rabbit alveolar macrophages which were treated at 0°C with phenylarsine oxide and then incubated at 37°C for 10 rain exhibited a two-to threefold increase in surface receptor activity for macroglobulin.protease complexes, diferric transferrin, and mannoseterminal glycoproteins. Analysis of the concentration-dependence of ligand binding indicated that changes in ligand-binding activity were due to changes in receptor number rather than alterations in ligand-receptor affinity. Surface receptor number could also be increased by treatment of cells with three other sulfhydryl reagents, N-ethylmalemide, p-chloromercurobenzoate, and iodoacetic acid. The increase in receptor activity was maximal after 10 min and decreased over the next hour. This decrease in cell-associated receptor activity was due to the release of large membrane vesicles which demonstrated a uniform buoyant density by isopycnic sucrose gradient centrifugation. Treatment of cells with phenylarsine oxide did not decrease the cellular content of lactate dehydrogenase or/~-galactosidase, indicating that cell integrity was maintained and lysosomal enzyme release did not occur. Our studies indicate that phenylarsine oxide treatment in the presence of extracellular Ca 2+ results in the fusion of receptor-containing vesicles with the cell surface.Studies indicate the existence of intracellular pools of plasma membrane receptors which can be recruited or exteriorized to the cell surface. These intracellular pools are thought to play a role in the recycling of membrane receptors. To date, intracellular pools of receptors have been demonstrated for asialoglycoproteins (1), mannose-terminal glycoproteins (2), insulin (3), transferrin (Tf) ~ (4) and a-macroglobulin, protease complex (aM-P) (5), but not for low density lipoprotein receptors in fibroblasts (6) or for asialoglycoprotein receptors in cultured hepatoma cells (7). Examination of thin sections of cells by electron microscopy using anti-receptor antibodies (8) or homogenization or cells followed by subcellular fractionation (4) indicates that the intracellular reservoir of asialoglycoprotein or Tf receptors is associated with a unique ~Abbreviations used in this paper: HBSS, Hanks' balanced salt solution; MAN-BSA, mannose-bovine serum albumin; MEM, minimal essential medium; aM.'ZSI-T, a-macroglobulin.~251-trypsin complex; aM-P, c~-macroglobutin, protease complex; NEM, N-ethylmalemide; PAO, phenylarsine oxide; PCMB, p-chloromercurobenzoate; Tf(Feh, diferric transferrin. low buoyant density organelle which may also contain recently internalized ligands. The biochemical properties of the intracellular compartment(s) containing the receptors are unclear.During a study of the effect of sulfhydryl reagents on endocytosis, we observed that treatment of alveolar macrophages with phenylarsine oxide (PAO), a vicinyl sulfhydryl reagent, resulted in an increase in the binding of a-macroglobulin. ~25I-trypsin complex (aM. 12~I-T) to cell surface receptors. In this study we found that treatment of macrophages...

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“…Cells fixed 30 min after exposure to A23187 and calcium still showed blebs and the unusual decorated microtubules. Although preincubation with colchicine (10 -5 M, 30 min) before the addition of A23187 and calcium decreased the total number of microtu-This capacity differs from that of diamide-treated PMN which also have a remarkably altered profile in thin section and in which a band of apparently contracted microftlaments is evident (24). FIGURE 2 (a) A higher magnification view of a portion of a cell treated as in Fig.…”

Section: Ionophore and Calciummentioning

confidence: 95%

Microfilaments and microtubules in calcium ionophore-induced secretion of lysosomal enzymes from human polymorphonuclear leukocytes.

Hoffstein¹,

Weissmann²

1978

The Journal of Cell Biology

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Human peripheral blood leukocytes (PMN) are induced to release lysosomal enzymes by the calcium ionophore A23187 in the presence but not the absence of extracellular Ca ++. Whereas secretion induced by particulate or immune stimuli is accompanied by an increase in visible microtubules and is inhibitable by colchicine, secretion induced by A23187 and Ca ++ was not accompanied by an increase in microtubule numbers and was not inhibited by colchicine. Ca ++ did not appear to regulate microtubule assembly in these cells since resting PMN had a mean of 22.3 --2.0 microtubules in the centriolar region as compared to 22.3 --1.1 in ionophore-treated cells and 24.9 _+ 1.5 in cells exposed to ionophore and 1 mM Ca ++. Bipolar filaments, 10 nm thick and 300-400 nm long, were numerous in the pericortical cytoplasm of cells exposed to both reagents. Microtubules in these cells were decorated with an electron-opaque fibrillar material. PMN exposed to A23187 and Ca ++ were contracted in two directions at right angles to each other: (a) Contractions parallel to the plasma membrane resulted in extensive plication of the cell membrane. The cytoplasm subjacent to the plicae contained dense filamentous webs. Plication was prevented by cytochalasin B or reversed by subsequent exposure to an endocytic stimulus such as zymosan. (b) Contractions perpendicular to the plasma membrane, toward the cytocenter, resulted in the formation of vacuoles in normal PMN and of membrane invaginations in cytochalasin B-treated PMN. Whereas contractions parallel to the plasma membrane could occur in the absence of enzyme release (ionophore alone) and enzyme release could occur in the absence of such contractions (ionophore plus calcium plus cytochalasin B), contraction toward the cytocenter occurred in all experimental conditions in which significant enzyme release was obtained. Thus, lysosomal enzyme secretion in PMN involves contractile movements of the plasma membrane toward the lysosomes rather than the reverse. These calcium-mediated contractile events are mediated by cytochalasin B-insensitive microfilaments but not by microtubule assembly.KEY WORDS microfilaments microtubules 9 calcium ionophore 9 secretion lysosomal enzymes human neutrophils 9 cytochalasin BThe motility of nonmuscle cells, including polymorphonuclear leukocytes (PMN), has been related to several morphologically and/or biochemi-J. CELL BIOLOGY 9 The Rockefeller University Press 9 0021-9525/78/0901-076951.00 769 on

show abstract

Lipid peroxidation and morphological changes in mammalian cells treated with the glutathione oxidant, diamide*1

Cited by 17 publications

References 22 publications

Thiol Oxidation-Induced Embryonic Cell Death in Mice Is Prevented by the Antioxidant Dithiothreitol1

Thiol Oxidation-Induced Embryonic Cell Death in Mice Is Prevented by the Antioxidant Dithiothreitol1

Phenylarsine oxide-induced increase in alveolar macrophage surface receptors: evidence for fusion of internal receptor pools with the cell surface.

Microfilaments and microtubules in calcium ionophore-induced secretion of lysosomal enzymes from human polymorphonuclear leukocytes.

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