Chromatin Condensation During Apoptosis Requires Atp

Kass, George E.N.; Eriksson, John E.; Weis, Marianne; Hinton, Richard H.; Orrenius, Sten; Chow, Sek C.

doi:10.1042/bst024569sa

Cited by 50 publications

(62 citation statements)

References 22 publications

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“…Although the morphological characteristics of apoptosis have been described in detail (Arends and Wyllie 1991), little is know about the mechanisms responsible for chromatin condensation except that it shows an absolute requirement for ATP, as recently reported by Kass et al (1996). In vitro, the ability of PA to condense DNA and to facilitate DNA conformational changes is well established (for review see Marton and Morris 1987).…”

Section: Discussionmentioning

confidence: 94%

Ultrastructural immunolocalization of polyamines in HeLa cells subjected to fast-freezing fixation and freeze substitution

Roch¹,

Nicolas

Quash³

1997

Histochemistry and Cell Biology

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Polyamines have been localized at the ultrastructural level in HeLa cells subjected first to fast-freezing fixation (FFF)-freeze substitution (FS) and then to an immunocytochemical method combining anti-polyamine antibodies and immunogold labelling. Polyamines were found in both the cytoplasm and the nucleus and, in the latter, particularly over the dense chromatin area. To our knowledge, this is the first example of the electron microscopic localization of a hapten after FFF-FS. For the preservation of fine ultrastructural details, this FFF-FS method is not only adequate but also greatly reduces, if not totally eliminates, any leeching-out and redistribution of the polyamines during the preparation of the sample. For the preservation of antigenicity in situ during FS, epoxy resin was more effective than hydrophilic LR white resin, probably due to the solubility of polyamines in the latter.

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Section: Discussionmentioning

confidence: 94%

Ultrastructural immunolocalization of polyamines in HeLa cells subjected to fast-freezing fixation and freeze substitution

Roch¹,

Nicolas

Quash³

1997

Histochemistry and Cell Biology

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“…[6][7][8][9][10][11] Severe (but not complete) depletion of ATP resulted in that certain typical apoptotic stimuli initiated necrosis instead of apoptosis, [7][8][9][10][11] whereas complete ATP exhaustion gave rise to a third type of cell death differing from both apoptosis and necrosis ("energy catastrophe"). 11 This indicates that not only apoptosis but also necrosis requires some ATP.…”

Section: Atp-dependent Steps Of Apoptosismentioning

confidence: 99%

Bioenergetic aspects of apoptosis, necrosis and mitoptosis

2006

Apoptosis

363

271

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In this review I summarize interrelations between bioenergetic processes and such programmed death phenomena as cell suicide (apoptosis and necrosis) and mitochondrial suicide (mitoptosis). The following conclusions are made. (I) ATP and rather often mitochondrial hyperpolarization (i.e. an increase in membrane potential, delta psi) are required for certain steps of apoptosis and necrosis. (II) Apoptosis, even if it is accompanied by delta psi and [ATP] increases at its early stage, finally results in a delta psi collapse and ATP decrease. (III) Moderate (about three-fold) lowering of [ATP] for short and long periods of time induces apoptosis and necrosis, respectively. In some types of apoptosis and necrosis, the cell death is mediated by a delta psi-dependent overproduction of ROS by the initial (Complex I) and the middle (Complex III) spans of the respiratory chain. ROS initiate mitoptosis which is postulated to rid the intracellular population of mitochondria from those that are ROS overproducing. Massive mitoptosis can result in cell death due to release to cytosol of the cell death proteins normally hidden in the mitochondrial intermembrane space.

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“…Lack of energy converts apoptosis to necrosis [16,17]. The release of cyto-c from mitochondria, observed in both the apoptotic initiation pathways (intrinsic and extrinsic), should promote impairment in the oxidative phosphorylation process in relation to the amount of cyto-c released into the cytosol.…”

Section: Commentmentioning

confidence: 99%

“…The existence of the cytosolic NADH/cyto-c electron transport pathway was uncovered in 1991 [11] before the finding reported in 1996 that, in physio-pathological conditions, cyto-c can be released into the cytosol where it becomes a fundamental component of the apoptotic cell death program [15]. Thereafter we proposed, and continue to maintain, that in apoptotic cells, with an increased level of cyto-c in the cytosol and the impairment of the respiratory chain, the activity of the NADH/cyto-c system, coupled with the generation of an electrochemical proton gradient [12,13], may represent an additional but necessary source of energy required for the correct execution of the death program [16,17]. Very recently we have reported that in liver mitochondria along with the release of cyto-c, ceramide, a well known inducer of apoptosis, promotes, the stimulation of the cytosolic NADH/cyto-c electron transport activity coupled with an increased generation of DWm useful for ATP synthesis [18].…”

Section: Introductionmentioning

confidence: 96%

Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis

et al. 2011

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In valinomycin induced stimulation of mitochondrial energy dependent reversible swelling, supported by succinate oxidation, cytochrome c (cyto-c) and sulfite oxidase (Sox) [both present in the mitochondrial intermembrane space (MIS)] are released outside. This effect can be observed at a valinomycin concentration as low as 1 nM. The rate of cytosolic NADH/cyto-c electron transport pathway is also greatly stimulated. The test on the permeability of mitochondrial outer membrane to exogenous cyto-c rules out the possibility that the increased rate of exogenous NADH oxidation could be ascribed either to extensively damaged or broken mitochondria. Accumulation of potassium inside the mitochondria, mediated by the highly specific ionophore valinomycin, promotes an increase in the volume of matrix (evidenced by swelling) and the interaction points between the two mitochondrial membranes are expected to increase. The data reported and those previously published are consistent with the view that "respiratory contact sites" are involved in the transfer of reducing equivalents from cytosol to inside the mitochondria both in the absence and the presence of valinomycin. Magnesium ions prevent at least in part the valinomycin effects. Rather than to the dissipation of membrane potential, the pro-apoptotic property of valinomycin can be ascribed to both the release of cyto-c from mitochondria to cytosol and the increased rate of cytosolic NADH coupled with an increased availability of energy in the form of glycolytic ATP, useful for the correct execution of apoptotic program.

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Chromatin Condensation During Apoptosis Requires Atp

Cited by 50 publications

References 22 publications

Ultrastructural immunolocalization of polyamines in HeLa cells subjected to fast-freezing fixation and freeze substitution

Ultrastructural immunolocalization of polyamines in HeLa cells subjected to fast-freezing fixation and freeze substitution

Bioenergetic aspects of apoptosis, necrosis and mitoptosis

Valinomycin induced energy-dependent mitochondrial swelling, cytochrome c release, cytosolic NADH/cytochrome c oxidation and apoptosis

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