Organic Osmotic Effectors and Chromatin Structure

Buche, André; Colson, Pierre; Houssier, Claude

doi:10.1080/07391102.1990.10507831

Cited by 19 publications

(7 citation statements)

References 25 publications

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“…Previous studies (Buche et al, 1989(Buche et al, , 1990(Buche et al, , 1993 have confirmed this protection effect. Indeed, these compounds hinder chromatin precipitation induced by NaCl, KCI, CaCl2, or MgCl2 in vitro.…”

Section: Introductionsupporting

confidence: 68%

“…Reaching a sufficient level of phosphate charges neutralization to produce DNA precipitation thus requires a greater amount of cationic compound. This also explains the effects of glycine and taurine in the chromatin precipitation experiments of Buche et al (1989Buche et al ( , 1990Buche et al ( , 1993 and probably their presence in the euryhaline cells that are able to support osmotic stress.…”

Section: Resultsmentioning

confidence: 71%

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23Na NMR study of the effect of organic osmolytes on DNA counterion atmosphere

Flock

Labarbe

Houssier

1996

Biophysical Journal

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The effect of different organic osmolytes on the DNA counterion condensation layer has been investigated by 23Na NMR relaxation measurements. The zwitterionic compounds glycine, beta-alanine, 4-aminobutyric acid, and 6-aminocaproic acid have shown an increasing capacity to decrease the amount of sodium ions in the vicinity of the macromolecule. The experimental data have been correlated with the dielectric constant increase in their corresponding solutions and have been compared with the prediction of counterion condensation theory. Polyols (sorbitol and mannitol) did not display the same effect. These compounds largely increase the relaxation rate of sodium ions in the proximity of DNA, unlike the zwitterionic compounds. This probably results from a perturbation of the water dynamic around the macromolecule, of the primary or secondary hydration shell of the sodium nuclei involved, or both.

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Section: Introductionsupporting

confidence: 68%

Section: Resultsmentioning

confidence: 71%

23Na NMR study of the effect of organic osmolytes on DNA counterion atmosphere

Flock

Labarbe

Houssier

1996

Biophysical Journal

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“…Organic osmolytes stabilize proteins, counteracting the adverse effects of inorganic and organic ions [1,7,8,10,12,22,38,39]. Possibly, destabilization of proteins participates in the disintegration of apoptotic cells.…”

Section: Discussionmentioning

confidence: 98%

Cellular taurine release triggered by stimulation of the Fas(CD95) receptor in Jurkat lymphocytes

Läng

Madlung

Uhlemann

et al. 1998

Pfl�gers Archiv European Journal of Physiology

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One of the hallmarks of apoptosis is cell shrinkage which appears to be important for cell death. The mechanisms mediating cell volume decrease have, however, not been addressed. Mechanisms employed by swollen cells to decrease their cell volume include activation of ion transport pathways, such as ion channels and KCl cotransport, and release of cellular osmolytes, such as taurine, sorbitol, betaine and inositol. The present study has been performed to test for release of taurine. To this end Jurkat human T-lymphocytes were loaded with [3H]taurine and apoptotic cell death induced by triggering the Fas(CD95) receptor with monoclonal crosslinking antibody. Triggering the Fas(CD95) receptor led to a release of 60+/-5% of cellular taurine within 90 min. The release did not occur prior to 45 min. The release coincided with cell shrinkage as evidenced from forward scatter in FACS analysis and preceeded DNA fragmentation according to propidium iodide staining. The delay of taurine release was not influenced by exchange of medium and thus was not due to extracellular accumulation of a stimulator. The Fas(CD95)-induced taurine release, cell shrinkage and DNA fragmentation were blunted by lowering of ambient temperature to 23 degreesC. Following pretreatment of cells with Fas(CD95) antibody at 23 degreesC rewarming led to rapid taurine release, cell shrinkage and DNA fragmentation, indicating that the temperature-sensitive step is distal to the mechanisms accounting for the delay. Osmotic cell swelling led to an immediate release of taurine. In conclusion, Fas(CD95) triggering leads to delayed taurine release through a temperature-sensitive mechanism.

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“…Alternatively, the stability of chromosomal sized DNA may suffer from replacement of histones by inorganic cations leading to an increased frequency of DNA dsb. These effects of inorganic ions are offset by accumulation of compatible organic osmolytes, which are more compatible with chromatin structure (33).…”

Section: Discussionmentioning

confidence: 99%

Hyperosmolality in the form of elevated NaCl but not urea causes DNA damage in murine kidney cells

Kültz

Chakravarty

2001

Proc. Natl. Acad. Sci. U.S.A.

175

119

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This study demonstrates, by using neutral comet assay and pulsed field gel electrophoresis, that hyperosmotic stress causes DNA damage in the form of double strand breaks (dsb). Different solutes increase the rate of DNA dsb to different degrees at identical strengths of hyperosmolality. Hyperosmolality in the form of elevated NaCl (HNa) is most potent in this regard, whereas hyperosmolality in the form of elevated urea (HU) does not cause DNA dsb. The amount of DNA dsb increases significantly as early as 15 min after the onset of HNa. By using neutral comet and DNA ladder assays, we show that this rapid induction of DNA damage is not attributable to apoptosis. We demonstrate that renal inner medullary cells are able to efficiently repair hyperosmotic DNA damage within 48 h after exposure to hyperosmolality. DNA repair correlates with cell survival and is repressed by 25 M LY294002, an inhibitor of DNA-activated protein kinases. These results strongly suggest that the hyperosmotic stress resistance of renal inner medullary cells is based not only on adaptations that protect cellular proteins from osmotic damage but, in addition, on adaptations that compensate DNA damage and maintain genomic integrity. C ells adapt to osmotic stress by cell volume regulation and protection of protein structure, activity, and metabolism to maintain proper cell function. Such protective responses are necessary because osmotic stress alters cell volume, the concentration and stability of proteins, and the rate of biochemical reactions (1). Proteins are protected from osmotic stress by molecular chaperones and compatible organic osmolytes (2, 3). We recently showed that mouse renal inner medullary collecting duct (mIMCD3) cells respond to hyperosmotic stress by induction of cell cycle arrest, the tumor suppressor p53, and the growth arrest and DNA damage inducible proteins GADD45 and GADD153 (4,5). These responses are known hallmarks of signaling pathways that counteract DNA damage in mammalian cells (6, 7). DNA damage is defined as an alteration of DNA structure capable of causing cellular injury and reduction of viability or reproductive fitness of the organism (8). Thus, an induction of DNA repair pathways may be required to confer the high osmotic stress tolerance that is characteristic of renal inner medullary cells. However, in contrast to the wealth of knowledge about osmotic effects on cell volume and protein stability and function, little is known about the consequences of osmotic stress on DNA integrity in mammalian cells. Studies on several mammalian cell lines, including CHO cells (9), PAP-HT25 cells (10), human peripheral lymphocytes (11), and V79 cells (12), indicate that osmotic stress can lead to chromosomal aberrations. Such aberrations may be the consequence of an increased frequency of DNA double strand breaks (dsb) or result from an inhibition of constitutive DNA-repair mechanisms. Hyperosmotic stress inhibits inducible DNA repair pathways that are activated in response to ionizing radiation in some mammalian cell...

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Organic Osmotic Effectors and Chromatin Structure

Cited by 19 publications

References 25 publications

23Na NMR study of the effect of organic osmolytes on DNA counterion atmosphere

23Na NMR study of the effect of organic osmolytes on DNA counterion atmosphere

Cellular taurine release triggered by stimulation of the Fas(CD95) receptor in Jurkat lymphocytes

Hyperosmolality in the form of elevated NaCl but not urea causes DNA damage in murine kidney cells

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