The role of cytosolic Ca2+ in cell injury, necrosis and apoptosis

Trump, Benjamin F.; Berezesky, Irene K.

doi:10.1016/0955-0674(92)90037-d

Cited by 184 publications

(98 citation statements)

References 15 publications

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“…Of particular relevance in the current context is the reported ability of caffeine to increase intracellular levels of Ca2+ and cAMP (Somani & Gupta, 1988), induce chromatin condensatin (Schlegel & Pardee, 1987), inhibit the DNA repair mechanism (Selby & Sancar, 1990), bind to adenosine receptors (Daly et al, 1991) and activate p34cdC2 protein kinase (Steinmann et al, 1991). All of these mediators and biochemical events directly or indirectly participate in various stages seen in apoptosis (Gerschenson & Rotello, 1992;Trump & Berezesky, 1992;Kizaki et al, 1990;Duvall & Wyllie, 1986;Arends et al, 1990). Thus, we have postulated that caffeine may modulate or accelerate TNF cytotoxicity by altering the levels of cytosolic Ca2" and cAMP which may subsequently affect the activity of endonucleases, kinases or phosphatases required for apoptotic cell death.…”

Section: Discussionmentioning

confidence: 99%

Caffeine potentiates the lethality of tumour necrosis factor in cancer cells

Belizário

Tilly²,

Sherwood³

1993

Br J Cancer

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Summary In this study we have investigated the interaction of caffeine, a prototypic methylxanthine, and TNF on the induction of cell death in mouse and human cell lines during progression from G, to successive phases of the cell cycle. Exposure of cells to TNF (0.1-100 ng ml-) as single agent for 48 h caused low or no lethality. The rates of cell death increased significantly when cells cultured with TNF for 24 h were exposed to caffeine (2.5-20 mM). The magnitude of the enhancement by caffeine was TNF and caffeine dose-dependent. The most effective response to this combination was observed in the mouse cell lines, WEHI and L929, followed by the human cell lines, HeLa, A375 and MCF-7, respectively. In L929 cells, TNF treatment did not inhibit DNA synthesis during the first S phase of the cell cycle (20-24 h), but it did block the progress toward a second S phase, indicating the cells were arrested at G2 phase or mitosis. Caffeine had great enhancer effect on L929 cells exposed to TNF for 24 h, but the effect was reduced in cells with either less than 24 h or greater than 28 h of exposure. L929 cells stimulated with TNF died via apoptosis, as judged by both morphological criteria and the occurrence of internucleosomal DNA cleavage. Exposure of TNF-treated cells to caffeine caused a greater increase in the proportion of apoptotic cells as well as the extent of internucleosomal DNA fragmentation.

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Section: Discussionmentioning

confidence: 99%

Caffeine potentiates the lethality of tumour necrosis factor in cancer cells

Belizário

Tilly²,

Sherwood³

1993

Br J Cancer

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“…Emphasis is placed on Ca 2ϩ pathways because Ca 2ϩ can function as a pluripotent regulatory molecule. Conversely, prolonged exposure to elevated [Ca 2ϩ ] cyt can result in cell death (1,2). Trypanosome survival therefore depends upon redundant energy-dependent processes that carefully control cytosolic free Ca 2ϩ concentrations ([Ca 2ϩ ] cyt ) 1 (3)(4)(5)(6)(7)(8).…”

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confidence: 99%

Selective Transfer of Calcium from an Acidic Compartment to the Mitochondrion of Trypanosoma brucei

Xiong

Ridgley

Enis

et al. 1997

Journal of Biological Chemistry

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“…In addition, the permeabilization of plasma membrane caused by fipronil, as showed by ALT and AST data, could also contribute to the increase in intracellular Ca 2+ level. This increased cytosolic Ca 2+ can lead to activation of proteases, phospholipases and ion-dependent endonucleases (Trump and Berzesky 1992). The activation of proteases and phospholipases induces changes in the cytoskeleton and plasma membrane.…”

Section: Discussionmentioning

confidence: 99%