The requirement for and mobilization of calcium during induction by sodium ascorbate and by hydrogen peroxide of cell death

Sakagami, Hiroshi; Kuribayashi, Nobuyuki; Iida, Midori; Hagiwara, Takaaki; Takahashi, Hideo; Yoshida, Hiroshi; Shiota, Fukiko; Ohata, Hisayuki; Momose, Kazutaka; Takeda, Minoru

doi:10.1016/0024-3205(96)00071-9

Cited by 27 publications

(18 citation statements)

References 14 publications

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“…Apoptotic thyrocytes were readily detected after an exposure to 50 µM H 2 O 2 . At concentrations as low as 10-30 µM, H 2 O 2 was reported to act as a potent apoptotic inducer of rat thymocytes (Sakamoto et al 1996) or human HL-60 cells (Sakagami et al 1996). In contrast, induction of apoptosis of human lung adenocarcinoma cells required a much higher (1 mM) H 2 O 2 concentration (Kazzaz et al 1996).…”

Section: Discussionmentioning

confidence: 99%

H2O2 induces apoptosis of pig thyrocytes in culture

Riou¹,

Rémy²,

Rabilloud³

et al. 1998

Journal of Endocrinology

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Apoptosis might be involved in the reduction of the thyroid cell population in physiopathological situations such as goitre involution and autoimmune deleterious processes. Up to now, little attention has been paid to the apoptotic phenomenon in the normal thyroid gland the specialized metabolism of which is expected to generate reactive oxygen species. Indeed, thyroid cells have the capacity to synthesize H 2 O 2 . In this study, we have analyzed the capacity of H 2 O 2 to trigger apoptosis of pig thyrocytes in culture to try to determine whether thyrocytes exhibit a particular resistance to apoptosis induced by an oxidative stress. We show that exposure of thyrocytes cultured as monolayers to exogenous H 2 O 2 induced cell death with characteristics of apoptosis. The effect of H 2 O 2 was concentration-dependent; apoptotic cells were already observed after exposure to 50 µM H 2 O 2 . At high concentrations (millimolar range), H 2 O 2 exerted toxic effects leading to rapid cell disruption. Within the first hour after the onset of exposure to 50-300 µM H 2 O 2 , early signs of apoptosis, i.e. DNA fragmentation, appeared in a low (0·1-1%) but definite fraction of thyrocytes. The proportion of adherent cells exhibiting DNA fragmentation remained fairly constant after 6, 15 and 24 h. During the 24-h period, an increasing number of cells detached from the culture dish and up to 30-40% of cells in suspension displayed apoptotic features. The fraction of cells that lost contact with the culture dish amounted to up to 25% 24 h after addition of 300 µM H 2 O 2 .In conclusion, as reported for other cell types, low H 2 O 2 concentrations are capable of triggering apoptosis in thyrocytes cultured as monolayers. Thyrocytes that undergo apoptosis secondarily lose contact with neighbour cells and the substratum; cell detachment from the monolayer probably happens within 1-2 h after initiation of DNA fragmentation. Our data show that the apoptotic commitment can take place many hours after initiation of the oxidative stress.

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Section: Discussionmentioning

confidence: 99%

H2O2 induces apoptosis of pig thyrocytes in culture

Riou¹,

Rémy²,

Rabilloud³

et al. 1998

Journal of Endocrinology

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“…Modification of the intracellular concentration of calcium is an intracellular event frequently involved in the apoptotic process [15,37,38]. In this context, we have recently shown that the contact between MCF-7 cells and HUVEC induced an immediate and transient increase in HUVEC intracellular free calcium concentration [12].…”

Section: Discussionmentioning

confidence: 99%

Induction of Endothelial Cell Apoptosis by Solid Tumor Cells

Kebers

Lewalle

Desreux

et al. 1998

Experimental Cell Research

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Abstract:The mechanisms by which tumor cells extravasate to form metastasis remain controversial. Previous studies performed in vivo and in vitro demonstrate that the contact between tumor cells and the vascular wall impairs endothelium integrity. Here, we investigated the effect of breast adenocarcinoma MCF-7 cells on the apoptosis of human umbilical vein endothelial cells (HUVEC). TUNEL labeling, nuclear morphology, and DNA electrophoresis indicated that MCF-7 cells induced a two-to fourfold increase in HUVEC apoptosis. Caspase-3 activity was significantly enhanced. Neither normal cells tested (mammary epithelial cells, fibroblasts, leukocytes) nor transformed hematopoietic cells tested (HL60, Jurkat) induced HUVEC apoptosis. On the contrary, cells derived from solid tumors (breast adenocarcinoma, MDA-MB-231 and T47D; fibrosarcoma, HT 1080) had an effect similar to that of MCF-7 cells. The induction of apoptosis requires cell-to-cell contact, since it could not be reproduced by media conditioned by MCF-7 cells cultured alone or cocultured with HUVEC. Our results suggest that cells derived from solid tumors may alter the endothelium integrity by inducing endothelial cell apoptosis. On the contrary, normal or malignant leukocytes appear to extravasate by distinct mechanisms and do not damage the endothelium. Our data may lead to a better understanding of the steps involved in tumor cell extravasation.

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“…Consequent peroxidation causes a loss of membrane fluidity and receptor alignment, and may lead to cellular lysis [4]. ROS have also been implicated in the induction of apoptosis in some cell types [5,6]. They cause cell injury accompanied by changes in the intracellular concentrations of free calcium ([Ca 2+ ] i ) and cyclic adenosine monophosphate levels ([cAMP] i ) [7,8] …”

Section: Introductionmentioning

confidence: 99%

Prevention of Reactive Oxygen-Induced Endothelial Cell Injury by Blocking Its Process

Shimura

Yamaguchi²,

Kuzume³

et al. 1999

Eur Surg Res

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Endothelial cell (EC) injury induced by reactive oxygen species (ROS) was investigated and effects of Ca²⁺ channel blockers, agents which elevate intracellular cAMP levels ([cAMP]_i), and protein kinase inhibitors on H₂O₂-induced EC injury were analyzed using human umbilical vein EC cultures. Exposure to H₂O₂ increased intracellular Ca²⁺ levels and decreased [cAMP]_i. Ca²⁺ channel blockers, [cAMP]_i-elevating agents, and protein kinase inhibitors significantly inhibited H₂O₂-induced EC injury. Data suggest that H₂O₂-induced EC injury is mediated by extracellular Ca²⁺ influx, intracellular cAMP efflux, and intracellular signaling, each of which is blocked by Ca²⁺ channel blockers, [cAMP]_i-elevating agents, or protein kinase inhibitors. It is suggested that ischemia/reperfusion injury induced by ROS may be prevented by Ca²⁺ channel blockers, [cAMP]_i-elevating agents, and protein kinase inhibitors.

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The requirement for and mobilization of calcium during induction by sodium ascorbate and by hydrogen peroxide of cell death

Cited by 27 publications

References 14 publications

H2O2 induces apoptosis of pig thyrocytes in culture

H2O2 induces apoptosis of pig thyrocytes in culture

Induction of Endothelial Cell Apoptosis by Solid Tumor Cells

Prevention of Reactive Oxygen-Induced Endothelial Cell Injury by Blocking Its Process

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